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PUBLICATIONS 1. 2. 3. Meyer JS. Histological picture of cerebral oedema. McGill Med J 1945; 14: 293-302. Meyer JS. The thalamus. McGill Med J 1947; 16: 299-313. Meyer JS. Effects of diencephalic injury on consciousness. McGill University, Masters Thesis, 1948. Meyer JS, Hunter J. Behavior deficits following diencephalic lesions. Neurology 1952; 2: 112-130. Reprinted in Year Book of Neuro Neurosurg and Psychiat 1962. Meyer JS, Foley JM. The encephalopathy produced by extracts of eosinophil and bone marrow. J Neuropath Exp Neurol 1953; 12: 349-362. Trans Amer Neurol Assn 1952. Denny-Brown D, Meyer JS, Horenstein S. The significance of perceptual rivalry resulting from parietal lesion. Brain 1952; 75: 433-471. Brown EF, Meyer JS. Pheochromocytoma with rupture of an intracranial aneurysm. New Eng J Med 1952; 247: 671-672. Meyer JS, Foley JM, Campagna-Pinto D. Granulomatous angiitis of the meninges in sarcoidosis. Arch Neurol Psychiat 1953; 69: 587-600. Denny-Brown D, Meyer JS, Fang HCH. Effects of vascular occlusion on cortical oxygen tension. Fifth International Neurol Cong, Lisbon 1953. Progress Reports to Bureau of Medicine and Surgery, Department of the Navy. a ; Report on U.S. Navy Head Injury Project, Acute Phase. Report to Surgeon General, October 1, 1953. Research Project N.M. 007088.11. Clinical Studies of the Reaction to Injury, December 31, 1953. Research Project N.M. 007091.09. Physiological Studies of the Reaction of the Brain to Injury.
Most members had a 2-tier copay benefit with a lower copayment for generic drugs and a higher copayment for brand-name formulary drugs. Fewer than 20% of members were enrolled in 3-tier copay drug benefit designs. The medical group did not assess if there were changes in the individual drug plans offered to the health plan members of the various employers. The medical group examined the options for managing the growth in drug expenditures, including early termination of the 3-year risk contract or requesting the educational assistance of the clinical and administrative staff of the health plan. Ultimately, the medical group elected a self-management option that involved creation of a data warehouse and use of these data in a prescriber education intervention. The medical group hired a clinical pharmacist to analyze drug utilization and assist in the creation of education tools to use with physician-prescribers. Educational interventions with prescribers were designed at year-end 1998 to blunt the increase in drug costs incurred by health plan members assigned to the medical group. The medical group was interested in the analysis of the impact of the intervention on average cost per claim prescription ; and utilization. ss Methods A retrospective pretest and posttest design was used to compare the results of the medical group with national data on drug cost and utilization. During 1998, the pharmacist studied the communication infrastructure of the group and the lines of authority. An analysis of drug utilization was commenced. The interventions in physician education regarding observed versus desired prescribing patterns began in January 1999. It was not possible to assess the education intervention in a prospective manner with a control group within the medical group because the medical group used electronic mail extensively for group discussion and held regular monthly meetings. It was also not possible to test the intervention against another large primary care practice in the region since there was not a comparable primary care group in the region with a global risk contract. The option for analysis was comparison with national composite data for the same time period. The Novartis Pharmacy Benefit Report, 1999 and 2000 editions, was chosen for benchmark comparative data.3, 4 The medical group was composed of 65 physicians: 50 internists, 14 pediatricians, and 1 family practitioner, distributed among 24 practice sites. This mix of primary care physicians 77% internists ; resulted in a member population that had a higher proportion of older adults who would contribute to higher PMPY drug cost than national averages for primary care groups that contained a higher percentage of pediatricians and family practitioners. Drug utilization data were only available for patients in global risk contracts so a comparison to risk and nonrisk patients was not possible. The 1999 and 2000 editions of the Novartis Pharmacy Benefit, for example, betahistine mesilate.
HBV and HCV infections are global public health problems [Lavanchy, 2003] worldwide seroprevalence: HBsAg 5% ; and anti-HCV 1% ; [Roussos et al., 2003] 400 million and 170 million persons chronically infected with HBV and HCV, resp. [Lai et al., 2003; Poynard et al., 2003] Italian study 526 Kosovar refugees ; [Chironna et al., 2001; Chirona et al., 2003] HBV infection seems to be at intermediate level of endemicity low prevalence of anti-HCV antibodies 0.7% ; Greek study among 130 refugees [Roussos et al., 2003] 13.4% HBsAg and 53.1% anti-HBc high endemicity ; higher among refugees from Albania and Asia anti-HCV antibodies: low extended epidemiological surveys are needed.
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Duration of treatment The optimal duration of PEP is unknown. However, animal studies and a case-controlled study of healthcare workers suggest that four weeks is required to minimise the potential for HIV transmission. It is recommended therefore that four weeks of PEP should be utilised unless source-testing after initiation of PEP determines that the "donor" is HIV negative or if it transpires that the recipient is, unknowingly already infected.
Require therapy that provides long-term control of parathyroid hormone concentrations without increasing calcium and phosphorus concentrations. Cinacalcet modulates the calcium-sensing receptor on the parathyroid gland to reduce secretion of parathyroid hormone and lower serum calcium, phosphorus and calcium-phosphorus product in haemodialysis patients. Methods. Dialysis patients with secondary hyperparathyroidism [parathyroid hormone PTH ; level 300 pg ml] who were enrolled in one of four phase 2 placebocontrolled studies were eligible to enrol in an open-label extension study in which all patients received cinacalcet. For this extension study, cinacalcet was initiated at 30 mg in all patients and the dose was escalated to a maximum of 180 mg once daily if PTH concentrations were 250 pg ml. Use of concomitant vitamin D sterols and phosphate binders was not restricted. Results. The analysis of all patients n 59 ; completing 100 weeks of cinacalcet treatment showed long-term control of PTH and calcium-phosphorus product. Approximately 55% achieved a PTH concentration 300 pg ml at the week-100 study visit, and 60% had at least a 30% reduction in PTH from baseline. Serum calcium, phosphorus and the calciumphosphorus product did not increase during the study. Concomitant vitamin D sterol and phosphate binder therapy remained stable. Cinacalcet was safe and generally well tolerated at doses up to 180 mg day. Conclusions. In this long-term study, cinacalcet effectively sustained reductions in PTH for up to 3 years without increasing concentrations of serum calcium, phosphorus or calcium-phosphorus product. The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. 561. A high peritoneal large pore fluid flux causes hypoalbuminaemia and is a risk factor for death in peritoneal dialysis patients - Heaf J.G., Sarac S. and Afzal S. [J.G. Heaf, Graevlingestien 9, 2880 Bagsvaerd, Denmark] - NEPHROL. DIAL. TRANSPLANT. 2005 20 10 ; - summ in ENGL Background. Hypoalbuminaemia is common in peritoneal dialysis PD ; patients and has an associated high mortality. An excess morbidity and mortality has previously been found in patients with high peritoneal transport. A high peritoneal large pore fluid flux JvL ; results in increased peritoneal loss of protein that possibly contributes to patient morbidity. Alternatively, hypoalbuminaemia and high transport status could be just a marker of capillary pathology associated with atherosclerotic comorbidity. Methods. Peritoneal dialys is capacity computer modelling of peritoneal transport, based on Rippe's three-pore model, was performed to measure JvL in 155 incident PD patients 2-4 weeks after PD initiation. Patient clinical and biochemical status was determined -6, -3, -1, 1 and 6 months after PD initiation, and every 6 months thereafter. JvL was redetermined in prevalent patients 2 and 4 years after PD initiation. Results. JvL was 0.106 0.056 ml min 1.73 m2 median 0.094, interquartile range 0.068-0.128 ; . It was correlated to age P 0.05; P 0.01; P 0.001 ; 2030 years 0.079 0.04; 70 years 0.121 0.071 ; , but not to gender. No correlation to diabetic or preexisting renal replacement therapy was seen, but patients with atherosclerosis had higher JvL 0.123 0.06 vs 0.100 0.056 ; as had patients with other systemic disease 0.121 0.68 vs 0.100 0.051 ; . JvL was positively correlated to area parameter r 0.41 ; , and negatively correlated to plasma albumin -0.36 ; . Patients were divided into three equal groups: group 1, JvL 0.075 ml min 1.73 m2 ; group 2, 0.075-0.11; group 3: 0.11. There was no difference between the groups in p-albumin prior to PD. Immediately after PD start, differences between the three groups appeared 1 month p-albumin: mol l ; group 1, 548 83; group 2, 533 86; group 3, 497 78 ; , and persisted for up to 6 years. No significant change in JvL was seen at 2 and 4 years. Patients with significant albuminuria also had hypoalbuminaemia 1 g day: 546 81 mol l; 2 g day: 503 54 mol l ; . Intermittent PD ameliorated the effect of JvL on albumin losses and clearance. Mortality was increased significantly with raised JvL , independently of age 2 year mortality: Group 1, 10%, group 3, 32% ; . There was no overall effect on technique survival, but hypoalbuminaemic group 3 patients had a higher failure rate . Conclusion. JvL is related to hypoalbuminaemia and mortality after PD initiation. A high JvL seems to be a marker of preexisting vascular pathology, and to cause hypoalbuminaemia after PD initiation. It is suggested that peritoneal albumin loss can have an identical pathogenic effect as urinary albumin loss, by Section 28 vol 66.2 and bethanechol, because where to buy betahistine.
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The promise of atypical antipsychotics fewer side effects mean enhanced compliance and improved functioning leslie citrome, md, mph; jan volavka, md, phd vol 116 no 4 october 2004 postgraduate medicine cme learning objectives to become familiar with the advantages that first-line second-generation antipsychotics have over first-generation antipsychotics to understand the different formulations and indications available for first-line second-generation antipsychotics to recognize that interindividual differences are important in the efficacy and tolerability of second-generation antipsychotics dr citrome has consulted for, received honoraria from, and or conducted clinical research supported by abbott, astrazeneca, bristol-myers squibb, lilly, janssen, novartis, pfizer, and repligen.
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| Because it doubles mortality 4 ; . It has been thought that at least 1 5 of CHF patients has AF 4, 5 ; . Similar data we obtained from our large series of 340 patients with pulmonary edema, most pronounced type of "left heart" CHF 6 ; . An interesting difference exists between practice where we are witnesses of association of CHF and AF every day ; and medical publications which mention CHF usually among less important causes of AF, and sometimes CHF is missing ; . This, obviously wrong opinion, was corrected by new data from Framingham study 7 ; . Namely, CHF increases chances for AF even 4.5 times in men ; to 5.9 times in women ; . It seems that CHF is not only among important factors for AF, but most important one 7 ; ! The influence of AF upon left ventricle LV ; function can be very pronounced, which was very nicely illustrated by Brill in 1938. y. He stated that "AF may cause CHF without any other heart disease and that following AF cease, recovery may be complete and long lasting" 8 and zebeta.
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Women simply "know" better, but rather in the question of how one knows, which types of knowledge are privileged, and why. Moving from the Woman Question in Regulation to the Regulatory Question in Feminism48 Like science in general, regulation involves gathering knowledge about the world, determining what is true, what the problems are, and how best to solve them. The question for feminists is how to develop a regulatory epistemology which does not reproduce the objectifying and dominating qualities of science or regulation as usual. I have tried to show that activists' claims of "knowing" as women what is best for all women results in a totalization and objectification of diverse women's needs and experiences not unlike the regulatory system they critique, one that observes women from a population-control perspective, a view from above which aims to govern women's bodies rather than facilitate their self-determination. Of course regulators must make decisions based on some generalization if they are to accomplish anything at all. I do not wish to argue that no woman's health activist, no scientist, no one can say anything about anyoneas Mohanty writes, "these arguments are not against generalization as much as they are for careful, historically specific generalizations responsive to complex realities" 2003: 37 ; . Feminist epistemology as articulated by women's health activists and feminist theorists points beyond the project of inviting "a few women" to speak on panels, and even beyond claims for an essentially, inherently preferable woman's standpoint.
Sheerin IG, Green FT, Sellman JD. Drug Alcohol Rev. June 2003. Vol.22. No.2. p.159-67. Reviewed by Dr Helen Moriarty.
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