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AlbenzaMichael J. Lambert, MD, RDMS Chad A. Harswick, MD Department of Emergency Medicine, University of Illinois College of Medicine Chicago, Illinois Correspondence: Michael J. Lambert, MD, RDMS Clinical Assistant Professor, Department of Emergency Medicine, University of Illinois College of Medicine Fellowship Director, Emergency Ultrasound Resurrection Medical Center 7435 W. Talcott Ave Chicago, Illinois 60631 mlambert62 mac Office 773-594-8574 Fax 773-594-7980 ABSTRACT A young man presented to the emergency room in extremis and deteriorated into a state of pulseless electrical activity. Bedside echocardiography by emergency medicine physicians was crucial to the clinical decision to implement thrombolytic therapy for suspected massive pulmonary embolus. INTRODUCTION Pulmonary embolism PE ; , a leading cause of death in the United States resulting in 200, 000 deaths per year, can rapidly progress to fatality.1, 2 Ten percent of patients with PE will die within the first hour of the event.1 The clinical presentation of PE ranges from nonspecific symptoms to severe shock and even death, primarily. The Gq family includes four members identified by their subunits as Gq, G11, G14, and G15 16 39 ; . These proteins are functionally similar yet multiple members of the Gq family are usually co-expressed in the same cells 39 ; . This has led to several investigations aimed at examining whether the various members of the Gq family, most notably Gq and G11, display distinct functional coupling to receptors or whether they are functionally interchangeable with multiple receptors. For example, Gq and G11, because valle di susa. 23. Douville RN, Bastien N, Li Y, Pochard P, Simons FER, HayGlass KT. Human metapneumovirus elicits weak IFN- memory responses compared with respiratory syncytial virus. J Immunol 2006; 176: 5848-55. Sampson HA, Munoz-Furlong A, Campbell RL, Simons FER et al. Second symposium on the definition and management of anaphylaxis: Summary report B Second National Institute of Allergy and Infectious Disease Food Allergy and Anaphylaxis Network symposium. J Allergy Clin Immunol 2006; 117: 391-397. Rawas-Qalaji MM, Simons FER, Simons KJ. Fast-disintegrating sublingual tablets: effect of epinephrine load on tablet characteristics. AAPS PharmSciTech 2006: 7 e-journal ; : Article 41. aapspharmsci ; . 26. Simons FER. Life-saving epinephrine not available for those in need. In Lowenstein H, Bienenstock J, Ring J editors ; : From Genes to Phenotypes. The Basis of Future Allergy Management. Hogrefe & Huber Publishers, Cambridge, MA, 2006: 218-219. 27. Akdis CA, Akdis M, Bieber T, Simons FER, et al, for the EAACI AAAAI PRACTALL Consensus Group. Diagnosis and treatment of atopic dermatitis in children and adults. J Allergy Clin Immunol 2006; 118: 152-69. Bousquet J, Van Cauwenberge P, Ait Khaled N, Simons FER, et al. Pharmacologic and anti-IgE treatment of allergic rhinitis. ARIA update in collaboration with GA2LEN ; . Allergy 2006; 61: 108696. Rawas-Qalaji MM, Simons FER, Simons KJ. Epinephrine for the treatment of anaphylaxis: Do all 40 mg sublingual epinephrine tablet formulations with similar in vitro characteristics have the same bioavailability? Biopharm Drug Dispos 2006; 27: 427-35. Custovic A, Simons FER. Drugs used in paediatric allergy: should we conduct studies in children or extrapolate from adults? Clin Exp Allergy Rev 2006; 6: 1-5. Thottingal TB, Stefura BP, Simons FER, Bannon GA, Burks W, HayGlass KT. Human subjects without peanut allergy demonstrate T cell-dependent Th2-biased, peanut-specific cytokine and chemokine responses independent of Th1 expression. J Allergy Clin Immunol 2006; 118: 905-14. Lieberman P, Camargo CA Jr, Bohlke K, Jick H, Miller RL, Sheikh A, Simons FER. Epidemiology of anaphylaxis. Ann Allergy Asthma Immunol 2006; 97: 596-602. Sheikh A, Shehata Y, Brown SGA, Simons FER. Adrenaline for the treatment of anaphylaxis with and without shock. Cochrane Database Syst Rev 2006; 4: CD006312. Albenza antiviralAlbenza information
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We also suggest that 1 ; product package inserts be written at an appropriate level for most readers; 2 ; promotions not use technical graphs and charts or pseudoscientific jargon; 3 ; promotions provide just as much attention to side effects as they do to treatment effects; 4 ; advertisements be less "drugcentric" and more "disease medical conditioncentric"; and 5 ; the industry enter into more nonproprietary partnerships with health communication researchers to develop a better understanding of how people process DTC advertising information and to devise strategies to communicate more effectively with consumers. n The government. The FDA can increase the likelihood of effective self-regulation through strong, well-funded, and aggressive oversight. The FDA also should take the lead in providing accurate, unbiased information to consumers. 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Reviews of these studies indicate that the recreational drug use of AZT recipients and controls is never reported, probably because HIV is thought to be the only cause of their ailments. These reviews also suggest that there is a hierarchy of openess toward AZT toxicity in AIDS papers: AZT is accepted as a red cell killer, causing anemia. It is less readily accepted as a killer of neutrophils, because neutropenia is immunodeficiency which AZT is said to prevent. AZT is least likely to be described as a lymphocyte or even T-cell killer, because these are the presumed targets of the hypothetical T-cell killer HIV, which AZT is supposed to inhibit. Therefore, evidence for lymphocytopenia and T-cell depletion is usually not mentioned or is hidden in the raw data of AIDS papers. The following analyses of AZT toxicity were made with these experiences in mind: 1. The licensing study of AZT, sponsored by the NCI and Burroughs Wellcome, the manufacturer of the drug, investigated 289 patients from AIDS risk groups with prior Pneumocystis pneumonia and unexplained weight loss, fever, oral candidiasis, night sweats, herpes zoster, and diarrhea Fischl et al., 1987; Richman et al., 1987 ; . All but 13 of these patients were males, but there was no information about their sexual orientation or recreational drug use. The study was planned for six months but was interrupted after four months because by then the therapeutic benefits of AZT were claimed to be too obvious to continue the placebo control. By that time only 1 out of 145 in the AZT group, but 19 out of 137 in the placebo group, had died. Therefore the study concluded that AZT can decrease mortality. However, during the same time period the lymphocyte counts had decreased over 50% in 34% of the AZT recipients, but in only 6% of the control group. In the AZT group, 66 suffered from severe nausea, compared to only 25 in the control group; muscle atrophy was observed in 11 AZT recipients but in only 3 from the control group. Moreover, 30 out of the 145 in the AZT group depended on multiple transfusions to survive anemia, compared to only 5 out of the 137 in the placebo group. Thus, the number of subj ects in the AZT group who would have died from severe anemia if untreated was larger i.e., 30 ; than the AIDS deaths and anemias of the control group combined, namely 19 + 5. The decreased mortality claim is further compromised by numerous concomitant medications other than transfusions for AZT-specific diseases and failure to match the AZT and placebo groups for the cumulative effects of prior and parallel recreational drug use. In addition, some of the AZT-specific AIDS diseases observed in the placebo group appear to be due to patient-initiated drug sharing between AZT and placebo recipients Lauritsen, 1990; Duesberg, 1992b; Freestone, 1992 ; and falsification of the case report forms Lauritsen, 1992; Hodgkinson, 1996 ; . Moreover, the low mortality of 0.7% 1 145 ; claimed by the licensing study for the first four months on AZT could not be extended in a followup study, which found the survival benefits of AZT rapidly declining after the original four month period. By 18 months, 32% of the original AZT group had died, compared to 35% of the former control group, which by then had also received AZT for 12 months Fischl et al., 1989 ; . The possibility that recreational drugs were the cause of AIDS, in which case anti-viral AZT would only be a fatal poison - like chemotherapy without cancer - was not even mentioned by the many authors of the AZT study. However, one of them, Durack, was the first to propose in 1981 that 'recreational drugs [are] immunosuppressive' Durack, 1981 ; . Another antiviral therapist, Donna Mildvan, had j ust published that a history of heavy or moderate use of nitrite inhalant before study entry was predictive of ultimate progression, for instance, albenza.
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