Non-physician providers vs. Foundation Health Plan--a major restraint-of-trade case study.
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Biomedical subjects
Publications and source records attributed to P Kelly.
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In this single centre prospective, double blind study, 98 patients with suspected acute myocardial infarction (AMI) were randomized, within six hours, to nifedipine 10 mg (46 patients) or placebo (52 patients) both administered sublingually. The delay time from onset of chest pain to treatment was 3.33 +/- 0.2 hours (mean +/- SEM) and 3.28 +/- 0.18 hours for the nifedipine and placebo treated groups, respectively. Treatment was continued orally for 3 days. AMI was confirmed in 28 patients given nifedipine and 23 patients given placebo. Infarct sizing by CK-MB isoenzyme release was possible, for technical reasons, in only 23 patients on nifedipine and 17 patients on placebo. CK-MB isoenzyme release was 710 +/- 104 IU l-1 and 655 +/- 118 IU l-1 for the nifedipine and placebo treated groups respectively (P greater than 0.05). In the acute coronary insufficiency (ACI) group--18 patients given nifedipine and 29 patients given placebo--there was no significant difference in duration of admission, urgent cardiac readmission or progression to AMI within one month. Study withdrawal occurred in 15.3%--8 nifedipine and 7 placebo. Overall, one month mortality was 10.2% with 5 deaths in both the nifedipine and placebo treated groups. Early treatment with nifedipine did not reduce enzymatically determined infarct size or one month mortality in patients with AMI, or reduce one month morbidity or mortality in patients with ACI.
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The present study was designed to assess the occurrence of small airways disease (SAD) in non-smoking sarcoidosis patients by pulmonary function measurement; and to investigate the possible mechanisms of SAD by measuring the in vitro production of arachidonic acid metabolites (PGE2 and LTB4) by peripheral blood mononucleocytes from sarcoidosis patients. SAD did in fact occur in 15 of the 32 sarcoid patients studied. The increase in LTB4 and decrease in PGE2 observed in SAD patients could imply a causative role for these arachidonic acid metabolites in SAD.
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A series of cross-linked, swellable polymers was sythesized from monomers such as acrylic acid, methacrylic acid, and others with various cross-linking agents to produce a range of polymers differing in charge densities and hydrophobicity. The densities, rate, and extent of hydration of the polymers were determined. An increase in the number of hydrophobic groups in the polymer structure reduced hydration whereas the density of the polymer was unaffected. A sensitive in vitro method for measuring adhesion of polymer to tissue from the rabbit stomach was developed. Polymers of acrylic acid loosely cross-linked (0.3%, w/w) with three different agents, divinyl glycol, 2,5-dimethyl-1,5-hexadiene, and divinylbenzene, showed the same degree of bioadhesion while poly(methacrylic acid-divinylbenzene) showed reduced bioadhesion. The small percent of cross-linking agent, irrespective of physicochemical properties, did not contribute substantially to bioadhesion, whereas the starting monomer had a large effect. The effect of pH on the bioadhesion of poly(acrylic acid-divinyl glycol) was studied at constant temperature, ionic strength, and osmolality. The polymer showed maximum adhesion at pH 5 and 6 and a minimum at pH 7. Gastrointestinal transit studies of cross-linked polymers in rats were studied. Poly(acrylic acid-divinyl glycol) and poly(methacrylic acid-divinylbenzene) were shown to have substantially longer GI transit times than the control, Amberlite 200 resin beads. The delay in transit time was due to bioadhesion of the polymer to the mucin-epithelial cell surface which was clearly observable on animal autopsy. The acrylic acid polymer showed a longer GI transit time than the methacrylic acid polymer, and this in vivo GI transit result is consistent with in vitro bioadhesion test results.
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The height and weight measurement of 928 young people of Busselton were collected over a period of up to 11 years. The prevalence of obesity was low in early childhood and increased progressively through adolescence and adulthood, so that 9% of male subjects and 16% of female subjects aged 21 years or over, were obese. The prevalence and degree of obesity were both greater in female subjects than in male subjects. Although most obese young adults were not obese in childhood, 50% of those who were obese between the ages of 9 and 14 years were still obese when examined in young adult life, and were at greater risk of becoming obese adults than were their non-obese peers. Most subjects who subsequently became obese young adults were significantly heavier than their non-obese peers at all ages from the age of 6 years.
RU 16117, the 11 alpha-methoxy derivative of ethynyl estradiol, is an orally active weak estrogen potentially effective in the treatment of estrogen-deficiency in postmenopausal women (climacteric symptoms and severe osteoporosis). Biochemical studies have shown that RU 16117, like estriol, possesses the properties characteristic of a partial estrogen agonist/antagonist. RU 16117 binds to the cytosol estrogen receptor (ER) to form a complex which dissociates much faster than the estradiol complex. This explains its lower nuclear uptake. Furthermore, the nuclear RU 16117 complex also dissociates faster than the estradiol complex. Consequently, although low doses of RU 16117 can induce the majority of the effects of estradiol (increased polymerase A and B activities, cytosol ER replenishment, progestin receptor induction, increased uterine weight), these effects are long-lived only if the dose is considerably increased or if the compound is administered repeatedly or continuously. Since RU 16117 transiently occupies available estrogen binding sites, it can prevent the full response of estradiol. Thus, under appropriate kinetic conditions, it acts as an estrogen antagonist on the above parameters and also on DMBA-induced mammary tumors in the rat. At a daily dose of 24 micrograms for a period of 4 weeks RU 16117 led to 65% reduction in the number of already-established tumors. RU 16117 inhibits basal gonadotropin secretion and decreases the LH response to LHRH. Injection of 5 micrograms s.c. to the rat in estrus markedly inhibited the spontaneous peaks of LH, FSH and PRL measured on the afternoon of expected proestrus. Low doses which block ovulation by 100% had no detectable effect on vaginal cornification, thus suggesting a greater sensitivity at the hypothalamo-pituitary level.(ABSTRACT TRUNCATED AT 400 WORDS)
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This article considers novel aspects to plant development. It starts by outlining the concept of plastic development. It then discusses polarity in plants arguing for the vascular tissue and surrounding cells as a major internal polar axis. The requirement for a change in polarity in this system when regeneration occurs is discussed and molecular mechanisms for specification and changing of polarity are outlined. The process of abscission is then discussed as an example of plastic development and it is concluded that many factors control abscission. Molecular changes in abscission zone cellulase are summarized and the notion of two phases in abscission are developed and generalized to other systems of development in plants.
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Transmural electrical stimulation and exposure to incubation media where some or all of the Na+ had been replaced with K+ were used to elicit transmitter release. Changes in noradrenaline content and ultrastructure of the nerve terminal varicosities in rat vas deferens were measured. Electrical stimulation in the presence of 4-aminopyridine had little effect, but high [K+] solutions caused a parallel reduction in noradrenaline content and the number of small dense-cored vesicles; large dense-cored vesicles showed no change, and small clear vesicles increased in number. In spite of a reduction in total vesicle number there was no evidence of expansion of the varicosity membrane. The parallel fall in noradrenaline content and in the number of small dense-cored vesicles suggests that the latter are the source of the released noradrenaline under the conditions of high [K+] stimulation we have used.
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Choroid plexus blood flow (CPBF) and glucose utilization (CPGU) were measured in two groups, each of seven identically prepared, unanesthetized rats, using complementary quantitative autoradiographic techniques. Both CPBF and CPGU were lowest in the lateral ventricles (0.83 +/- 0.01 . g-1 . min-1 and 0.70 +/- 0.02 mumoles . g-1 . min-1, respectively) and highest in the fourth ventricle (1.56 +/- 0.05 ml l g-1 . min-1 and 1.39 +/- 0.05 mumoles . g-1 . min-1, respectively). Despite this heterogeneity, the proportionate relationship between CPBF and CPGU was relatively constant throughout the ventricular system. This suggests that blood flow and metabolism may normally be coupled in the choroid plexus, and that the choroid plexus of the fourth ventricle may account for a disproportionate share of the functional activity of this tissue.
We have previously shown that brief periods of high frequency synaptic stimulation of the rat hippocampus influence the endogenous phosphorylation of a 40,000 Mr brain protein (Browning et al.). The results of the present study demonstrate that this brain phosphoprotein is enriched in a purified mitochondrial fraction and co-migrates with the alpha-subunit of pyruvate dehydrogenase in sodium dodecyl sulfate polyacrylamide gels. Comparisons of total and partial proteolytic fingerprints indicate that the two proteins are essentially identical. In addition, the phosphorylation of the 40,000 Mr brain protein is sensitive to both dichloroacetate and magnesium as has been reported for pyruvate dehydrogenase. Taken together these data provide persuasive evidence that the brain protein is the alpha-subunit of pyruvate dehydrogenase and thereby raise the possibility that even very short periods of synaptic activity influence an enzyme of particular importance to mitochondrial metabolism in brain.
Dimethylbenz(a)anthracene (DMBA)-induced mammary tumors in the rat are well known to be hormono-dependent. Daily injections of an LHRH agonist, [D-Ala6, des-Gly-NH2(10)]LHRH ethylamide (LHRH-A), 1 microgram daily, for 38 days results in a 35% decrease in the number of tumors present at the beginning of the experiment compared to a decline of 45% after ovariectomy and of 8% in the control group. This is accompanied by a marked reduction in ovarian LH and FSH receptors. LHRH-A treatment also resulted in reduction in the number of progesterone and prolactin receptors in the tumors. In addition, an increase in plasma LH and FSH and a decline in plasma prolactin (PRL) concentrations are observed. The mechanisms by which the LHRH agonist induces its antitumoral effect probably relate to an ovarian desensitization to LH and FSH with a concomitant decrease in circulating levels of estrogen and prolactin, two well known stimuli for the growth of DMBA-induced mammary tumors.