The political economy of responsibility in health and illness.

This article addresses the question: to what extent do health care strategies in a given political economy increase people's perceptions of responsibility to take charge of their health, but do not structurally empower them to satisfy their health needs. In shaping health care policies, societies typically adopt one of three broad strategies, linking their larger political economy and modes of exercising power: a marketplace strategy, a state-managerial strategy or a national participatory strategy. Because of their different arrangements of structural power, these strategies result in three very different approaches to responsibility for health and illness. Changes in the political economy of health in Nicaragua during the Somoza, Sandinista and Chamorro periods illustrate the changing fields of choice within which care-seekers must make their health care decisions.

Selected characteristics of graduate medical education in the United States.

For the second year, the Department of Data Systems in the Medical Education Group of the American Medical Association gathered information on graduate medical education primarily by means of an electronic data collection system. Eighty-eight percent of 6622 programs surveyed responded, with 83% reporting detailed information on residents. Analysis of graduate medical education data shows that the number of residents increased by 34.9% from the academic years 1980-1981 to 1990-1991, while the number of graduate year 1 residents decreased by 2%. In the same decade, the proportion of women residents increased by 7.1%. The number of minorities in graduate medical education has grown, but their proportions within the total resident population have remained largely unchanged. The number of graduates from schools of osteopathic medicine has increased by 265% over the same 10-year period. Between 1989 and 1990, a 31.6% increase was recorded in the number of international medical graduates in graduate year 1 residency positions; most of this increase (63.4%) occurred among noncitizens of the United States.

Graduate medical education in the United States.

The annual surveys of residency programs on which this report is based have had a higher than 90% response rate for the 5 years previous to 1989. Because of a change to the new electronic data collection system in 1989, the response rate decreased to 78.3%. To adjust for the lower response rate, a regression model computed from data from previous years was developed that permitted projected estimates for 1989 data. These numbers are included in several key tables. The number of GY-1 positions seems to have decreased for 1990, although this may be an artifact of the response rate. Reported unfilled positions, including GY-1 unfilled positions, have increased each year since 1985. The number of new-entry residents (GY-1) seems to be leveling out after decreasing since 1985. Because of the lower response rate, it is difficult to determine the trend in the total number of residents on duty. While the observed number of residents is lower than in 1988, statistical projections indicate an increase of 5% over the 1988 count. Thirty-nine percent of residents were training in family practice, internal medicine, or pediatrics. The number and percent of women in residency programs has remained relatively stable despite a steady increase in the number of women graduating from US medical schools. The percentage of FMG residents has continued to decrease. The percentage of black non-Hispanic residents remains steady. The number of graduates of osteopathic medical schools in ACGME programs has increased 17% since 1987. The number of institutions involved in graduate medical education has not changed significantly during the past 3 years.

Words of power: personal empowerment and healing.

This paper examines instances of ritual use of words in a diverse selection of alternative healing groups in a modern society. These words are distinguished by their users' belief that they are endowed with a power, an effectiveness, separate from and in addition to their literal meaning. Three specific features of ritual language contribute to its effectiveness: (1) its function as an objectification of power, (2) its transformative functions--especially its metaphoric and metonymic usages, and (3) its performative aspects. This paper argues that one of the key factors in healing illness is mobilizing resources of power, especially enhancing the ill person's sense of personal empowerment. Ritual language use in alternative healing is one of the foremost elements in this empowerment, because it both represents and objectifies power. Within a belief system in which they are significant, words of power indeed have the power to effect healing.

Enhanced breakdown of bovine articular cartilage proteoglycans by conditioned synovial medium in vitro: a possible role for prostaglandins.

Addition of conditioned medium derived from fragment cultures of synovium dissected from bovine knee joints (SM) to cultures of articular cartilage derived from the same animal resulted in a significant increase in breakdown of cartilage proteoglycans, measured as the release of [35S]sulphate from pre-labelled cartilage pieces. Culturing the synovium in the presence of indomethacin (indo-SM) at a concentration of 1.4 x 10(-5) mol/l reduced the breakdown-enhancing effect of the SM in some but not in all of the experiments. Addition of prostaglandins E1 or E2 (PGE1 or PGE2) (2.8 x 10(-7)-1.4 x 10(-5) mol/l) together with indo-SM resulted in a significant enhancement of breakdown of cartilage proteoglycans. PGA1, PGB1 and PGF2 alpha(less than 1.5 x 10(-5) mol/l) had, however, no effect in this system. Neither PGE1, PGE2 nor indomethacin at the concentrations mentioned above had any direct effect on breakdown of cartilage proteoglycans. No difference was found between the breakdown enhancing capacity of SM derived from synovium cultured in the presence of indo plus PGE1 or PGE2 (less than 4 x 10(-5) mol/l) and indo-SM. These findings are discussed in terms of cellular interactions.

Enhanced breakdown of bovine articular cartilage proteoglycans by conditioned synovial medium in vitro. The effect of glucocorticoids and protein synthesis inhibitors.

Addition of conditioned synovial medium (SM) from cultured calf knee-joint synovium to cultures of articular cartilage from the same animal resulted in a significant increase in breakdown of cartilage proteoglycans. Culturing the synovium in the presence of glucocorticoids (hydrocortisone, dexamethasone, prednisolone) or protein synthesis inhibitors (cycloheximide or actinomycin D) reduced the breakdown effect. In contrast, enhancement of proteoglycan breakdown was observed when the cartilage was exposed to glucocorticoids in the presence of SM from synovium cultured without these drugs (control SM). The stimulatory effect on cartilage breakdown of control SM or control SM + glucocorticoids was markedly reduced in the presence of actinomycin D or cycloheximide. The authors conclude that glucocorticoids under certain conditions enhance cartilage degradation and therefore, although they exert the temporary anti-inflammatory effects, treatment of joint diseases with glucocorticoids may not be beneficial in the long-term.

Enhanced breakdown of bovine articular cartilage proteoglycans by conditioned synovial medium. The effect of serum and dextran sulphate.

Medium from cultured bovine synovial membrane when applied to articular cartilage from the same animal enhanced proteoglycan breakdown, as measured by the release of [35S]sulphate from prelabelled cartilage, principally by activating chondrocytes to secrete or activate their own enzymes. This effect persisted whether or not the synovium was cultured in medium containing fetal calf serum. The release of proteoglycans from cartilage was markedly enhanced when the synovium was cultured in the presence of dextran sulphate (200 micrograms/ml), while dextran sulphate had no effect upon cartilage alone or when added together with medium cultured in the absence of dextran sulphate. Since the release of the proteoglycan breakdown products from frozen and thawed cartilage was not stimulated by dextran sulphate, this agent appeared to be enhancing the indirect chondrocyte-mediated effect of synovial medium rather than the direct proteolytic enzyme-induced effect. A possible mechanism for the production of a substance responsible for the chondrocyte-mediated matrix degradation is proposed, involving monocyte-like or macrophage-like cells, either resident in the synovial tissue or derived from the circulation.

Production of collagenase and inhibitor (TIMP) by normal, rheumatoid and osteoarthritic synovium in vitro: effects of hydrocortisone and indomethacin.

1. The amounts of latent and active collagenase and of collagenase inhibitor (TIMP) produced by two normal, three rheumatoid and two osteoarthritic synovial specimens in culture were compared. Normal synovia produced TIMP, but little latent enzyme. Rheumatoid synovia produced higher levels of total collagenase activity than normal, of which up to 50% in one sample was present in the medium in an active form, whereas no specific inhibitory activity due to TIMP was detectable. The amounts of collagenase and TIMP produced by osteoarthritic synovia were more variable and appeared to reflect the degree of inflammation in the tissue at the time of initiating the cultures. 2. Concentrations of TIMP were usually higher in the culture media of normal, rheumatoid and osteoarthritic synovia when hydrocortisone was present. Correspondingly, amounts of total collagenase were reduced. Production of prostaglandin E (PGE) were inhibited in a dose-dependent manner by hydrocortisone. 3. Indomethacin had no consistent effect on the production of TIMP by rheumatoid and osteoarthritic synovia, although it tended to depress production of collagenase. The production of TIMP by normal synovia was depressed by indomethacin. No PGE was detectable in the media when indomethacin was present. 4. These results are consistent with those from previous animal studies, and we conclude that the balance between production of collagenase and TIMP may be critical in determining the extent of the destructive processes in arthritis. The ability of hydrocortisone to suppress production of collagenase and to increase free TIMP concentration, as well as to inhibit synthesis of prostaglandin, may explain in part how the drug exerts its therapeutic effects in patients with rheumatoid arthritis.

Characterization of collagenase, other metallo-proteinases and an inhibitor (TIMP) produced by human synovium and cartilage in culture.

1. Explants of human synovium from normal, rheumatoid and osteoarthritic subjects produced proteinases in culture that could degrade connective tissue macromolecules at neutral pH. 2. The proteinases detected in the media were predominantly of the class requiring metal ions for activity, and occurred in either partially or wholly latent forms. Activation could be achieved by treatment with either trypsin or the organo-mercurial, 4-aminophenylmercuric acetate. 3. Explants of both normal and osteoarthritic synovium produced an inhibitor of collagenase in the early days of culture, similar to that previously described for rabbit tissues. In contrast, no free inhibitor could be detected in the media of rheumatoid synovial cultures. 4. Explants of normal human articular cartilage produced latent collagenase and free inhibitor in culture. 5. These findings suggest that the activity of tissue-derived metallo-proteinases may be controlled by locally synthesized inhibitors, by mechanisms analogous to those already described for rabbit model systems. Changes in the synthesis and degradation of inhibitor could be important in human diseases in which destruction of connective tissue is a prominent feature.

The effects of anti-inflammatory drugs on prostaglandin production by rheumatoid synovial tissue.

The effect of anti-inflammatory drugs on prostaglandin production by rheumatoid synovial tissue has been investigated. Synovial explants were maintained in tissue culture for periods up to six days and PGE2 concentrations in culture were determined by radioimmunoassay. The more potent nonsteroidal inhibitors of PGE2 production and their IC50 (micrometer) values were indomethacin 0.005, flufenamic acid 0.2, flurbiprofen 0.6, ibuprofen 2.0 , naproxen 6.0, phenylbutazone 10.0, and aspirin 20.0. Drugs with weak or insignificant effects were hydroxychloroquin, acetaminophen, azathioprine, chloroquin, penicillamine, gold Na thiomalate, and Na salicylate. Glucocorticoids were potent inhibitors; dexamethasone 0.003, prednisolone 0.01, hydrocortisone 0.03; while mineralocorticoids deoxycorticosterone and aldosterone were inactive at 1.0 micrometer. There is a reasonably good correlation between the IC50 concentrations of the nonsteroidal inhibitors and their peak free plasma concentration achieved during therapy in man. Inhibition of prostaglandin synthesis may contribute to the effects of many but not all anti-inflammatory drugs.

Prostaglandin synthesis by rheumatoid synovium and its stimulation by colchicine.

The synthesis of prostaglandins by rheumatoid synovial tissue in organ culture was studied utilizing radioimmunoassay, with antisera to PGB1, PGF1alpha and PGF2alpha. It was established that PGE2 and PGF2alpha were the major prostaglandins formed by analyses of culture media with the two antisera to PGF, before and after alkali treatment. Indomethacin at 5 mug/ml suppressed prostaglandin synthesis, usually to less than 1% of control cultures. Colchicine, 0.1 mug/ml resulted in marked stimulation of prostaglandin synthesis, in some cases over 10 fold. It is suggested, because of the colchicine effect, that the state of the microtubules may regulate the rate of prostaglandin biosynthesis. It is possible that prostaglandin E2 produced by rheumatoid synovia may contribute to the pathogenesis of the inflammatory reaction and lead to destruction of juxta-articular bone in rheumatoid arthritis.