Abstract Purpose Using the Delphi process, a panel of experienced preceptors achieved consensus on best practices to increase preceptor efficiency and effectiveness. Methods The Delphi panelists completed 3 survey rounds and a face-to-face meeting. Survey questions covered several topics, including preparation of students for rotations, preceptor efficiency and effectiveness, potential resident contributions to precepting, methods of developing critical-thinking skills and providing assessment and feedback, precepting time metrics, and barriers to preceptor effectiveness. Panel consensus was defined as agreement of ≥80%. Results Fifteen of 36 invited preceptors (42%) completed all 3 survey rounds. The expert panel reached consensus on 6 essentials for effective rotations, 8 precepting contributions that could be made by appropriately trained residents, precepting barriers, 4 strategies for teaching critical thinking, and 5 valuable characteristics of the One Minute Preceptor model. Panelists reported on time spent with students presenting new patient cases (median, 10 minutes per case), time devoted to assessment of students’ clinical performance (median, 22 minutes per student weekly), and time dedicated to student professional development (median, 20 minutes per student weekly). Conclusion Important strategies for preceptors identified by the panel included (1) a thorough orientation to logistics, expectations, and scheduling of activities, (2) using appropriately trained residents in student training, (3) providing opportunities for critical thinking and therapeutic decision-making, (4) giving frequent, quality feedback on clinical activities, and (5) giving feedback to learners on a regular basis.
Familial combined hyperlipidemia (FCHL) was first described as an autosomal dominant inherited trait with primary action on triglyceride levels and secondary effects on cholesterol metabolism. This conclusion has since been questioned by several groups despite subsequent supportive biochemical and metabolic studies. To reexplore the genetics of FCHL, we assembled 55 families from the United Kingdom comprising 559 persons ascertained through probands with both hypercholesterolemia and hypertriglyceridemia. The results of univariate complex segregation analysis were consistent with a major gene acting on triglyceride and explaining two thirds of the genetic variability and 20% of the phenotypic variance in triglyceride levels. Univariate analysis did not identify a major genetic component acting on cholesterol levels. Bivariate segregation analysis rejected a major gene model. We also reexamined the original FCHL pedigrees collected by Goldstein et al and obtained results similar to those in the UK families. The prospects for mapping putative major genes determining triglyceride levels in FCHL patients by linkage analysis are discussed.
Journal Article RFLP for the human apollpoprotein B gene: II;EcoRI Get access L. Priestley, L. Priestley Molecular Medicine Research Group, MRC Clinical Research CentreWatford Road, Harrow, Middlesex HAI 3UJ Search for other works by this author on: Oxford Academic PubMed Google Scholar T. Knott, T. Knott Molecular Medicine Research Group, MRC Clinical Research CentreWatford Road, Harrow, Middlesex HAI 3UJ Search for other works by this author on: Oxford Academic PubMed Google Scholar S. Wallis, S. Wallis Molecular Medicine Research Group, MRC Clinical Research CentreWatford Road, Harrow, Middlesex HAI 3UJ Search for other works by this author on: Oxford Academic PubMed Google Scholar L. Powell, L. Powell Molecular Medicine Research Group, MRC Clinical Research CentreWatford Road, Harrow, Middlesex HAI 3UJ Search for other works by this author on: Oxford Academic PubMed Google Scholar R. Pease, R. Pease Molecular Medicine Research Group, MRC Clinical Research CentreWatford Road, Harrow, Middlesex HAI 3UJ Search for other works by this author on: Oxford Academic PubMed Google Scholar J. Scott J. Scott Molecular Medicine Research Group, MRC Clinical Research CentreWatford Road, Harrow, Middlesex HAI 3UJ Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 13, Issue 18, 25 September 1985, Page 6790, https://doi.org/10.1093/nar/13.18.6790 Published: 25 September 1985
To discuss prevention and management of adverse drug reactions which result from antiretroviral use in patients infected with HIV. There are four classes of antiretroviral agents used in the treatment of HIV/AIDS. Side effects to medications are common place and often difficult to avoid. In many cases, research is not able to identify the exact cause of an event. The severity of adverse reactions varies greatly, and some may be difficult to manage; typically, prevention is more desirable than treatment. However, this is not always true. This paper will review class-wide and individual side effects from antiretrovirals and, in some cases, the mechanism of action that results in the event. Class-wide side effects for nucleoside/tide reverse transcriptase inhibitors (NRTIs) include lactic acidosis, peripheral neuropathy and lipoatrophy. Adverse reactions from individual NRTIs, such as abacavir-induced hypersensitivity reactions, will also be discussed. Class-wide side effects to non-nucleoside reverse transcriptase inhibitors include rash and hepatotoxicity, while efavirenz has its own unique CNS reactions. Protease inhibitor side effects include hyperglycemia, lipoaccumulation, dyslipidemia, and gastrointestinal (GI) intolerance. We will also review specific side effects caused by indinavir, ritonavir, and atazanavir. Finally, adverse reactions from the fusion inhibitor, enfuvirtide, will be mentioned.Antiretrovirals are an important break-through in the treatment of HIV/AIDS. However, adverse reactions from these drugs can range from mild to life-threatening, and determining which agent is the cause is frequently difficult to discern. Fortunately, side effects can be monitored, treated and in many cases, prevented.
HIV infection is epidemic with over 39.5 million people infected worldwide. Protease inhibitors (PIs) remain the mainstream therapy for the treatment of HIV infection. At the 2006 International AIDS Society conference it was reported that patients who receive PIs as part of their therapy show a trend toward shorter virologic failure times as well as significant increases in CD4+ cell count. Similar results are reported in a case ‐ control study in which significantly increased CD4+ cell counts are measured in patients receiving PIs as part of their Highly Active Anti Retroviral Therapy (HAART) compared to those receiving Non ‐ Nucleoside Reverse Transcriptase Inhibitor (NNRTI) therapy. As the molecular mechanisms explaining these clinical observations are still unknown, basic scientific studies leading to the understanding of how PIs enhance T cell activation would allow for more effective therapeutic management. During a viral infection, T ‐ cells are first activated through the T ‐ cell receptor complex which induces the expression of the cytokine interleukin 2 (IL ‐ 2) and the IL ‐ 2 high affinity receptor, CD25. IL ‐ 2 induces both autocrine and paracrine activation of T ‐ cells, resulting in clonal expansion and differentiation, and ultimate viral clearance. Apart from CD25, several other cell surface markers are upregulated during T ‐ cell activation including the adhesion molecule CD38; the signal transmitting receptor CD69; and the antigen presenting complex, HLA ‐ DR. While previous attempts to show changes in T ‐ cell surface markers due to PI treatment have been unsuccessful, we show for the first time that the PI, lopinavir (lop) increases CD25+ T ‐ cell levels, independent of viral load.
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