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We previously demonstrated the importance of the surface area burden as the key dose metric in the elicitation of inflammation in rat lungs by low-solubility, low-toxicity particles (LSLTP). We have now explored the dosimetry of LSLTP in vitro using epithelial cell interleukin (IL)-8 gene expression as a surrogate for potential of particles to cause inflammation. The proximal alveolar region (PAR) of the lung has been identified as a key site for the retention of respirable particles, as it receives high deposition but has slow clearance compared to the larger airways. For these reasons, a few days after exposure to particles the residual dose is concentrated in the PAR region. Re-expressing our rat lung data as particle surface area burden per unit of PAR surface area we obtained a threshold value for onset of inflammation of 1 cm2/cm2. We carried out dose responses in vitro for onset of IL-8 gene expression with the same particles as we had used in vivo. When we expressed the in vitro dose as surface area dose per unit A549cell culture surface area, we obtained a threshold of 1 cm2/cm2. This concordance between proinflammatory effects in vivo (PMN in BAL) and in vitro (epithelial IL-8 gene expression) confirms and supports the utility of the particle surface area metric and the importance of the PAR. These studies also open the way for future in vitro approaches to studying proinflammatory effects of a range of toxic particles based on sound dosimetry that complemenst animal use in particle toxicology. [ABSTRACT FROM AUTHOR]

Nanotechnology is involved with the creation and/or manipulation of materials at the nanometer (nm) scale, and has arisen as a consequence of the novel properties that materials exhibit within the "nano" size range. The attraction of producing, and exploiting nanoparticles (NPs; one dimension less than 100 nm) is a consequence of the fact that the properties are often strikingly different from bulk forms composed from the same material. As a consequence, the field of nanotechnology has generated substantial interest resulting in incorporation of NPs into a wide variety of products including electronics, food, clothing, medicines, cosmetics and sporting equipment. While there is general recognition that nanotechnology has the potential to advance science, quality of life and to generate substantial financial gains, a number of reports suggest that potential toxicity should be considered in order to allow the safe and sustainable development of such products. For example, substances which are ordinarily innocuous can elicit toxicity due to the altered chemical and physical properties that become evident within nano dimensions leading to potentially detrimental consequences for the producer, consumer or environment. Research into respirable air pollution particles (PM10) has focused on the role of ultra fine particle (diameter less than 100 nm) in inducing oxidative stress leading to inflammation and resulting in exacerbation of preexisting respiratory and cardiovascular disease. Epidemiological studies have repeatedly found a positive correlation between the level of particulate air pollution and increased morbidity and mortality rates in both adults and children. Such studies have also identified a link between respiratory ill health and the number of ambient ultrafine particles. In vivo and in vitro toxicology studies confirm that for low solubility, low toxicity materials such as TiO2, carbon black and polystyrene beads, ultrafine particles ar- - e more toxic and inflammogenic than fine particles. In many of these studies the term "ultrafine particle" can be directly exchanged for nanoparticle, as these particles are manufactured industrially. In such studies the NPs generate reactive oxygen species (ROS) to a greater extent than larger particles leading to increased transcription of pro-inflammatory mediators via intracellular signaling pathways including calcium and oxidative stress. To date, only limited NP compositions and structures have been tested, including materials such as carbon, polystyrene beads and TiO2 as surrogate particles that aimed to represent particulate air pollution. All of these materials are generally low toxicity and low solubility. Much work is required to identify whether the conclusions made for such materials can be extrapolated to engineered nanoparticles varying not only in size but also, shape, composition, structure, surface area, surface coating, and aggregation state. Therefore, it is necessary to reveal if the diversity of NPs available will confer to a varied extent and mechanisms of toxicity. [ABSTRACT FROM PUBLISHER]

The Social Vulnerability Scale (SVS), an informant-report of social vulnerability for older adults, was piloted in a sample of 167 undergraduate students (63 male, 104 female) from the University of Queensland. Participants aged 18A â'A 53 (MA =A 25.53 years, SDA =A 7.83 years) completed the SVS by rating a relative or friend aged â[0/00]50 years (MA =A 71.65 years, SDA =A 12.49 years): either someone with memory problems, stroke, dementia, or other neurological condition (nA =A 85); or a healthy older adult (nA =A 82). Excellent internal consistency and testA â'A retest reliability were demonstrated, and the SVS effectively differentiated healthy older adults from those with a neurological condition based on proxy ratings of social vulnerability. The SVS is a potentially useful adjunct measure of older adults' capacity to reside independently. [ABSTRACT FROM AUTHOR]

Ultrafine (Uf) particles are a component of particulate air pollution suggested to be responsible for the health effects associated with elevations of this pollutant. We have previously suggested that Uf particles, through the induction of oxidative stress, may induce inflammation in the lung, thus exacerbating preexisting illness in susceptible individuals. Alveolar macrophages are considered to play a key role in particle-mediated inflammation and lung disease. The effect of Uf particles on rat alveolar macrophages and human blood monocytes was investigated with reference to the roles of calcium and reactive oxygen species (ROS). TNF-α protein release, intracellular calcium concentration, TNF-α mRNA expression, and transcription factor activation were studied as end points after treatment of rat alveolar macrophages or peripheral blood monocytes. The calcium channel blocker verapamil, the intracellular calcium chelator BAPTA-AM, the calmodulin inhibitor W-7, and the antioxidants Trolox and Nacystelin (NAL) were included in combination with Uf particles. Verapamil reduced intracellular calcium concentration in rat alveolar macrophages on stimulation with Uf particles. This effect was also apparent with transcription factor AP-1 activation. All antagonists and antioxidants reduced Uf-stimulated nuclear localization of the p50 and p65 subunits of NF-κB in human monocytes. Verapamil, BAPTA-AM, and NAL reduced Uf-stimulated TNF-α protein release, whereas only verapamil reduced Uf-stimulated mRNA expression in rat alveolar macrophages. In human monocytes, verapamil, Trolox, BAPTA-AM, and W-7 reduced Uf-stimulated TNF-α protein release. These findings suggest that Uf particles may exert proinflammatory effects by modulating intracellular calcium concentrations, activation of transcription factors, and cytokine production through a ROS-mediated mechanism. reactive oxygen species; tumor necrosis factor-α. [ABSTRACT FROM AUTHOR]

The effects of PM10, one of the components of particulate air pollution, was investigated using human monocytes and a mouse macrophage cell line (J774). The study aimed to investigate the role of these nanoparticles on the release of the pro-inflammatory cytokine TNF-α and IL-1α gene expression. We also investigated the role of intracellular calcium signalling events and oxidative stress in control of these cytokines and the effect of the particles on the functioning of the cell cytoskeleton. We showed that there was an increase in intracellular calcium concentration in J774 cells on treatment with PM10 particles which could be significantly reduced with concomitant treatment with the calcium antagonists verapamil, the intracellular calcium chelator BAPTA-AM but not with the antioxidant nacystelyn or the calmodulin inhibitor W-7. In human monocytes, PM10 stimulated an increase in intracellular calcium which was reduced by verapamil, BAPTA-AM and nacystelyn. TNF-α release was increased with particle treatment in human monocytes and reduced by only verapamil and BAPTA-AM. IL-1α gene expression was increased with particle treatment and reduced by all of the inhibitors. There was increased F-actin staining in J774 cells after treatment with PM10 particles, which was significantly reduced to control levels with all the antagonists tested. The present study has shown that PM10 particles may exert their proinflammatory effects by modulating intracellular calcium signalling in macrophages leading to expression of pro-inflammatory cytokines. Impaired motility and phagocytic ability as shown by changes in the F-actin cytoskeleton is likely to play a key role in particle clearance from the lung. [ABSTRACT FROM AUTHOR]

Increases in the levels of environmental particulate matter (PM10) in the air are associated with a variety of adverse health effects, particularly in susceptible patients with chronic lung and cardiovascular diseases. The adverse effects in the lungs are probably caused by oxidative stress leading to lung inflammation. The expression of many genes, including those encoding pro-inflammatory mediators, involves the remodelling of the chromatin structure provided by histone proteins. Chromatin is tightly coiled around histone proteins and therefore the access of transcription factors to the transcriptional machinery is inhibited. Histone acetylation causes the unwinding of the chromatin structure, thereby allowing transcription factor access to promoter sites, whereas histone deacetylation has the opposite effect of winding chromatin and inhibiting transcription. Nuclear histone acetylation is reversible and is regulated by a group of histone acetyltransferases (HATs), which promote acetylation, and histone deacetylases (HDACs), which promote deacetylation. There are several co-activators, transcription factors and nuclear proteins that have HAT activity. The aim of this study was to determine whether the PM10-mediated mRNA expression and release of interleukin-8 (IL-8) from alveolar airspace epithelial cells is associated with histone acetylation and oxidative stress. We studied the effects of PM10 and an HDAC inhibitor (trichostatin-A, TSA) on the release of IL-8 by enzyme-linked immunosorbent assay, and the acetylation of histone 4 (H4) was assessed by immunocytochemistry in human alveolar type II cells. PM10 and H2O2 increased IL-8 protein release from A549 cells after 20 h treatment, and this was enhanced by HDAC inhibition (TSA co-treatment). PM10 and H2O2 treatment also increased the HAT activity. PM10 enhanced H4 acetylation, which was mediated by oxidative stress, as shown by thiol antioxidant inhibition. The PM10-and TSA-mediated increases in IL-8 and histone acetylation were associated with increases in nuclear factor-ΰB activation. These data suggest that the remodelling of chromatin by histone acetylation plays a role in the PM10-mediated pro-inflammatory responses in the lungs. This PM10 response is mediated by oxidative stress. [ABSTRACT FROM AUTHOR]

The mechanisms by which elevated levels of particulate air pollution increase the risk of cardiovascular (CV)-related deaths remain unclear. A role for plasma fibrinogen has been proposed with the suggestion that particle induced inflammation in the lung may stimulate an hepatic acute phase response and thereby increase plasma fibrinogen concentration, a known risk factor for CV disease. Human alveolar epithelial cells have been reported to synthesize fibrinogen and we therefore investigated the possibility that particle deposition may, through direct and indirect mechanisms, induce local alveolar production of fibrinogen. Here we present data to suggest that PM10 exposure could stimulate alveolar epithelial cell synthesis of fibrinogen indirectly, through the induction of inflammatory cytokines such as interleukin-6. Locally produced fibrinogen may exacerbate pulmonary inflammation and potentially contribute to systemic levels of plasma fibrinogen, thereby increasing the risk of CV responses in susceptible, PM10 exposed individuals. [ABSTRACT FROM AUTHOR]

Ultrafine particles have been suggested to be one of the components responsible for the adverse health effects of environmental particulate air pollution (PM10). This study aimed to investigate the ability of fine and ultrafine carbon black (ufCB) particles to stimulate production of the pro-inflammatory cytokine tumour necrosis factor alpha (TNFα) by primary rat alveolar macrophages. We have previously demonstrated that ufCB, but not fine CB, is able to enhance calcium influx into macrophages in the presence of a secondary calcium agonist such as thapsigargin. For this reason, we also investigated the role of intracellular calcium signalling in controlling ufCB-induced TNFα production. Observation of rat alveolar macrophages stained with the calcium-sensitive dye Fura-2 and then treated with ufCB resulted in a rapid but transient increase in cytosolic calcium concentration in individual cells within 15 min of exposure. ufCB treatment of the primary macrophages also induced a significant increase in TNFα mRNA and protein production within 4 h of exposure. Inhibition of calcium influx using a calcium channel blocker, verapamil, as well as inhibition of calcium signalling events with an intracellular calcium chelator, BAPTA-AM, both prevented the ufCB-induced increase in TNFα protein production. TNFα mRNA production was inhibited by verapamil but not by BAPTA-AM. Addition of the antioxidant nacystelin, previously shown to inhibit ufCB-induced calcium influx into macrophages, also inhibited TNFα protein but not mRNA production. These data support the hypothesis that ultrafine particles, via reactive oxygen species, enhance calcium influx into macrophages and that these oxidative and calcium signalling events activate TNFα production. [ABSTRACT FROM AUTHOR]

A range of different particle types cause excessive lung inflammation that is thought to play a role in the various types of pathology they produce. Recently attention has been focused on ultrafine particles and the phenomenon of rat lung overload. The authors and their collaborators have shown previously that the surface area metric drives the overload response. Acute inflammatory response following instillation of particles has also been used to evaluate hazard but has been criticized because of the non-physiological delivery and the problems of local overload. We have instilled a number of low-toxicity dusts of various particle sizes and assessed neutrophil influx into the lung at 18-24 h. The extent of inflammation has been shown to be a function of the surface area instilled. Since ultrafine particles present a 'special' case of high surface area, they are relatively inflammogenic. There is no evidence that ultrafine particles of carbon black, titanium dioxide or latex have any special reactivity in addition to their large surface area. We tested whether we could use this approach to model the reactivity of highly toxic dusts. Rats were instilled with either DQ12 quartz or aluminium lactate-treated DQ12 and, as anticipated, the high specific surface toxicity of DQ12 meant that it was much more inflammogenic than was predicted using the relationship described for low-toxicity dusts. By contrast, aluminium lactate-treated DQ12 fell on to the line of 'low-toxicity' dusts. This approach presents the possibility of modelling potential toxicity for nuisance dusts based on the inflammatory response of a given instilled surface area dose. [ABSTRACT FROM AUTHOR]

Increases in the levels of environmental particulate matter (PM10) in the air are associated with a variety of adverse health effects, particularly in susceptible patients with chronic lung and cardiovascular diseases. The adverse effects in the lungs are probably caused by oxidative stress leading to lung inflammation. The expression of many genes, including those encoding pro-inflammatory mediators, involves the remodelling of the chromatin structure provided by histone proteins. Chromatin is tightly coiled around histone proteins and therefore the access of transcription factors to the transcriptional machinery is inhibited. Histone acetylation causes the unwinding of the chromatin structure, thereby allowing transcription factor access to promoter sites, whereas histone deacetylation has the opposite effect of winding chromatin and inhibiting transcription. Nuclear histone acetylation is reversible and is regulated by a group of histone acetyltransferases (HATs), which promote acetylation, and histone deacetylases (HDACs), which promote deacetylation. There are several co-activators, transcription factors and nuclear proteins that have HAT activity. The aim of this study was to determine whether the PM10-mediated mRNA expression and release of interleukin-8 (IL-8) from alveolar airspace epithelial cells is associated with histone acetylation and oxidative stress. We studied the effects of PM10 and an HDAC inhibitor (trichostatin-A, TSA) on the release of IL-8 by enzyme-linked immunosorbent assay, and the acetylation of histone 4 (H4) was assessed by immunocytochemistry in human alveolar type II cells. PM10 and H2O2 increased IL-8 protein release from A549 cells after 20 h treatment, and this was enhanced by HDAC inhibition (TSA co-treatment). PM10 and H2O2 treatment also increased the HAT activity. PM10 enhanced H4 acetylation, which was mediated by oxidative stress, as shown by thiol antioxidant inhibition. The PM10-and TSA-mediated increases in IL-8 and histone acetylation were associated with increases in nuclear factor-κB activation. These data suggest that the remodelling of chromatin by histone acetylation plays a role in the PM10-mediated pro-inflammatory responses in the lungs. This PM10 response is mediated by oxidative stress. [ABSTRACT FROM AUTHOR]

Background: Controversy exists regarding who should provide care for those with HIV/AIDS. While previous studies have found an association between physician HIV experience and patient outcomes, less is known about the relationship of physician specialty to HIV/AIDS outcomes or quality of care.Objective: To examine the relationship between choice of appropriate antiretroviral therapy (ART) to physician specialty and HIV/AIDS experience.Design: Self-administered physician survey.Participants: Random sample of 2,478 internal medicine (IM) and infectious disease (ID) physicians.Measurements: Choice of guideline-recommended ART.Results: Two patients with HIV disease, differing only by CD4+ count and HIV RNA load, were presented. Respondents were asked whether ART was indicated, and if so, what ART regimen they would choose. Respondents' ART choices were categorized as "recommended" or not by Department of Health and Human Services guidelines. Respondents' HIV/AIDS experience was categorized as moderate to high (MOD/HI) or none to low (NO/LO). For Case 1, 72.9% of responding physicians chose recommended ART. Recommended ART was more likely (P <.01) to be chosen by ID physicians (88.2%) than by IM physicians (57.1%). Physicians with MOD/HI experience were also more likely (P <.01) to choose recommended ART than those with NO/LO experience. Finally, choice of ART was examined using logistic regression: specialty and HIV experience were found to be independent predictors of choosing recommended ART (for ID physicians, odds ratio [OR], 4.66; 95% confidence interval [95% CI], 3.15 to 6.90; and for MOD/HI experience, OR, 2.05; 95% CI, 1.33 to 3.16). Results for Case 2 were similar. When the analysis was repeated excluding physicians who indicated they would refer the HIV "patient," specialty and HIV experience were not significant predictors of choosing recommended ART.Conclusions: Guideline-recommended ART appears to be less likely to be chosen by generalists and physicians with less HIV/AIDS experience, although many of these physicians report they would refer these patients in clinical practice. These results lend support to current recommendations for routine expert consultant input in the management of those with HIV/AIDS. [ABSTRACT FROM AUTHOR]

Pratylenchus thornei densities were monitored in field plots of two winter wheat cultivars in a dry farming area of southern Spain. Samples were taken fortnightly during the wheat-growing season and from the following dry fallow. Under bread wheat cv. ‘Yecora’, densities of P. thornei increased for 5 to 6 months and then were maintained or slightly decreased thereafter, surviving the summer dry fallow in an anhydrobiotic state (78.2% and 85.3% survival in soil and roots, respectively). Under durum wheat cv. ‘Donpedro’, nematode densities decreased over the growing season, although densities within the roots increased during the first 2 months of the wheat-growing period, indicating that nematodes could penetrate the roots of this cultivar but were unable to reproduce. These observations suggest resistance of wheat cv. Donpedro to P. thornei. [ABSTRACT FROM AUTHOR]

Objectives: In July 1995 the Soufriere Hills volcano on the island of Montserrat began to erupt. Preliminary reports showed that the ash contained a substantial respirable component and a large percentage of the toxic silica polymorph, cristobalite. In this study the cytotoxicity of three respirable Montserrat volcanic ash (MVA) samples was investigated: M1 from a single explosive event, M2 accumulated ash predominantly derived from pyroclastic flows, and M3 from a single pyroclastic flow. These were compared with the relatively inert dust TiO(2) and the known toxic quartz dust, DQ12.Methods: Surface area of the particles was measured with the Brunauer, Emmet, and Teller (BET) adsorption method and cristobalite content of MVA was determined by x ray diffraction (XRD). After exposure to particles, the metabolic competence of the epithelial cell line A549 was assessed to determine cytotoxic effects. The ability of the particles to induce sheep blood erythrocyte haemolysis was used to assess surface reactivity.Results: Treatment with either MVA, quartz, or titanium dioxide decreased A549 epithelial cell metabolic competence as measured by ability to reduce 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). On addition of mannitol, the cytotoxic effect was significantly less with M1, quartz, and TiO(2). All MVA samples induced a dose dependent increase in haemolysis, which, although less than the haemolysis induced by quartz, was significantly greater than that induced by TiO(2). Addition of mannitol and superoxide dismutase (SOD) significantly reduced the haemolytic activity only of M1, but not M2 or M3, the samples derived from predominantly pyroclastic flow events.Conclusions: Neither the cristobalite content nor the surface area of the MVA samples correlated with observed in vitro reactivity. A role for reactive oxygen species could only be shown in the cytotoxicity of M1, which was the only sample derived from a purely explosive event. These results suggest that in general the bioreactivity of MVA samples in vitro is low compared with pure quartz, but that the bioreactivity and mechanisms of biological interaction may vary according to the ash source. [ABSTRACT FROM AUTHOR]

The role of explicit knowledge in the teaching and learning of a second language has been the subject of much research. Little of this, however, has taken place within the context of the Modern Foreign Languages in secondary school classrooms in the UK. In this study, we investigate the relationship between knowing and using the perfect tense in French in a small-scale project carried out over two years, involving a small group of learners. [ABSTRACT FROM AUTHOR]

Most theory of mind (ToM) tests are designed for subjects with a mental age of 4-6 years. There are very few ToM tests for subjects who are older or more able than this. We report a new test of ToM, designed for children 7-11 years old. The task involves recognizing faux pas. Study 1 tested 7-9, and 11-year-old normal children. Results showed that the ability to detect faux pas developed with age and that there was a differential developmental profile between the two sexes (female superiority). Study 2 tested children with Asperger syndrome (AS) or high-functioning autism (HFA), selected for being able to pass traditional 4- to 6-year level (first- and second-order) false belief tests. Results showed that whereas normal 9- to 11-year-old children were skilled at detecting faux pas, children with AS or HFA were impaired on this task. Study 3 reports a refinement in the test, employing control stimuli. This replicated the results from Study 2. Some patients with AS or HFA were able to recognize faux pas but still produced them. Future research should assess faux pas production. [ABSTRACT FROM AUTHOR]

The porphyrias, a group of rare acquired or hereditary diseases, are due to abnormalities in the haeme biosynthesis pathway. Clinical manifestations vary with the deficient enzyme. Porphyria cutanea tarda (PCT), the most common of the porphyrias, is the result of decreased function of the enzyme uroporphyrinogen decarboxylase. This is a deficiency that is limited to the liver more commonly in the acquired form; and involves other tissues, including erythrocytes, in the hereditary form. Clinical manifestations in this type of porphyria are limited to the skin1,2. Porphyria cutanea tarda has been reported in association with HIV infection 3-39. Here we present 2 cases of PCT in HIV-infected patients; in addition, the clinical characteristics and the epidemiology of PCT in HIV/AIDS patients is reviewed, and controversies regarding pathogenesis are discussed. [ABSTRACT FROM AUTHOR]

Objective: To gather qualitative data regarding HIV/AIDS patients' perspectives about HIV-1 protease inhibitors (PIs), and about their experiences taking and adhering to regimens containing PIs.Design: Six focus groups of persons under care for HIV were conducted between September and November 1996 regarding participants' knowledge, awareness, experiences when taking, and adherence to antiretroviral regimens containing PIs. An identical discussion guide was used to facilitate all six groups. Focus group proceedings were audiotaped, transcribed, coded for themes, and analyzed qualitatively.Setting: HIV/AIDS practices of three teaching hospitals and two community health centers.Patients/participants: Fifty-six patients with HIV disease: 28 men and 28 women.Measurements and Main Results: Knowledge and positive impressions of PIs were prevalent among this diverse group of persons with HIV, and did not differ by race/ethnicity or gender. Most knew that these were new, potent medications for treating HIV/AIDS. Networks of persons with HIV and medical providers were the most important information sources. Those taking PIs were aware that adherence to the regimen is important, and most were using special strategies to maximize their own adherence, but expressed considerable frustration about the central role these medication regimens had assumed in their life. A subset who did not believe they would adhere to these regimens had declined treatment with them. Motivating factors for taking and adhering to these complex regimens were improving CD4 counts and viral loads and the patient-provider relationship.Conclusions: Among those with HIV/AIDS, awareness of PIs and their effectiveness is substantial, owing to the impact of informal networks and medical providers. This early positive "reputation" of PIs may enhance motivation for adherence. Those who are taking PIs invest substantial effort adhering to these complex regimens, but resent the need to make medications the focus of their lives. [ABSTRACT FROM AUTHOR]

Objective: To examine the relation of patient characteristics and site of care to the perception of ambulatory care quality by persons with AIDS (PWAs).Design: Patient surveys and medical record review were used to determine PWAs' perceptions of their ambulatory care, self-perceived health status, primary care relationships, sociodemographic characteristics, and severity of illness.Setting: A public-hospital HIV clinic, an academic group practice, and a staff-model health maintenance organization (HMO) that together care for 20% of all Massachusetts PWAs.Patients: All active patients as of February 12, 1990, and all new AIDS patients at each of the three sites during the subsequent 13 months.Measurements and Main Results: The primary outcome measure was a six-item scale of patient-rated quality of care (PRQC), a newly developed measure that combined patients' ratings of their physician care, nursing care, involvement in medical decisions, and overall quality of care. Multiple logistic regression was carried out with low PRQC (lowest quartile) as the dependent variable, to identify correlates of patient perceptions of poor quality. Patients who had a primary nurse were significantly less likely to have low PRQC scores (OR = 0.50, 95% CI = 0.26 to 0.97). Black patients and patients who used injection drugs were significantly more likely to rate their care in the lowest quartile (OR = 2.22, 95% CI = 1.04 to 4.78; and OR = 2.43, 95% CI = 1.13 to 5.23, respectively), as were those who had lower self-perceived health status, after controlling for confounders; no association was found by site or severity.Conclusions: These results show that primary nursing may be an important determinant of how PWAs rate the quality of their ambulatory care. Furthermore, PWAs who are black or who are injection drug users are less satisfied than are others with the quality of their ambulatory AIDS care. [ABSTRACT FROM AUTHOR]