Articulation and integration in professional education curriculum.

[ES] El trabajo presenta la problemática suscitada durante el proceso de innovación curricular en la Facultad de Medicina de la Universidad de Chile, concerniente a la integración curricular y, especialmente, de los aprendizajes. Se discuten los aspectos conceptuales y se proponen lineamientos relacionados con diferentes maneras de instalar oportunidades de integración en los mapas curriculares. Se indican ejemplos de cómo diferentes planes de formación enfrentan la problemática.  [EN] This paper presents problematic issues that stemmed from the process of curriculum innovation at the Faculty of Medicine, of the University of Chile, concerning curricular and –specially– learning integration. Conceptual aspects are discussed and action lines are proposed concerning different ways of installing integration opportunities in curricular maps. Examples are offered about how different courses of study cope with this problem.Rojas Serey, AM.; Hawes Barrios, G. (2012). Articulación e integración en el currículum de formación profesional. REDU. Revista de Docencia Universitaria. 10(extra):55-81. https://doi.org/10.4995/redu.2012.6093OJS558110extra.Beckers, J. (2007). Compétences et identité professionnelles. L'enseignement et autres métiers de l'interaction humaine. Bruxelles (Belgique): Éditions de Boeck Université.Corleto, C., Kimball, J., Tipton, A., & MacLauchlan, R. (1996, 6‐9 Nov, 1996). Foundation Coalition First Year Integrated Engineering Curriculum at Texas A6M University‐ Kingsville: Development, Implementation and Assessment. Paper presented at the Frontiers in Education Conference., 26th Annual Conference, Proceedings., Salt Lake City, Utah.Dienstag, J. L. (2011). Evolution of the New Pathway Curriculum at Harvard Medical School: the New Integrates Curriculum. Perspectives in Biology and Medicine, 54(1), 36‐54.Gott, S. P. (1990). The assisted learning of strategic skills. In N. Fredericksen, R. Glaser, A. Lesgols & M. Shafto (Eds.), Diagnostic monitoring of skill and knowledge acquisition (pp. 173‐189). Hillsdale, NJ: Lawrence Erlbaum Associates.Hawes, G., & Rojas, A. M. (2012). Integración en el Currículum (pp. 21). Santiago: Departamento de Educación en Ciencias de la Salud, Facultad de Medicina, Universidad de Chile.Hawes, G., & Troncoso, K. (2009). Conceptualización de la competencia. Santiago: Universidad de Chile, Facultad de Medicina.Jonnaert, P., Masciotra, D., Barrette, J., Morel, D., & Mane, Y. (2007). From Competence in the Curriculum to Competence in Action. Prospects, 37(2), 187‐ 203.Le Boterf, G. (2000). Ingeniería de las competencias. Barcelona: Gestión 2000.Le Boterf, G. (2003). Ingénierie et Évaluation des Compétences. Paris: Éditions d'Organisation.Leblanc, S., Ria, L., Dieumegard, G., Serres, G., & Durand, M. (2008). Concevoir des dispositifs de formation professionnelle des enseignants á partir de l'analyse de l'activité dans un approche enactive. Activités. Revue electronique., 5(1).Maturana, H., & Varela, F. (1973). De Máquinas y Seres Vivos: Una teoría sobre la organización biológica. Santiago de Chile: Editorial Universitaria.Perrenoud, P. (2004). Diez nuevas competencias para enseñar. Barcelona: Editorial Graó.Sadovnik, A. R. (2001). Basil Bernstein (1924‐2000). Perspectivas: revista trimestral de educación comparada, XXXI (4), 687‐703.Troncoso, K., & Hawes, G. (2007). Esquema general para los procesos de transformación curricular en el marco de las profesiones universitarias. Santiago: Dirección de Pregrado, Vicerrectoría de Asuntos Académicos, Universidad de Chile.Varela, F. (1990). Conocer. Las ciencias cognitivas: tendencias y perspectivas. Cartografía de las ideas actuales. Barcelona: Gedisa.Varela, F. (1991). Ética y Acción. Conferencias italianas dictadas en la Universidad de Bolonia 16‐18 de Diciembre de 1991. Santiago: Dolmen.Varela, F. (2000). Four batons for the future of cognitive science. In B. Wiens (Ed.), Envisioning Knowledge: Dumont Cologne

Novel mutation in YMDD motif and direct neighbourhood in a child with chronic HBV-infection and clinical lamivudine and adefovir resistance - a scholarly case

<p>Abstract</p> <p>Context</p> <p>Chronic HBV infection is a major cause of hepatocellular carcinoma (HCC) which meanwhile has become the 5^thmost reason for a fatal outcome of cancer. Worldwide, approximately 350 million people are chronically HBV infected and as such of risk to develop HCC, of those an estimated high rate of children. Treatment of chronic infection is sufficient to reduce the rate of HCC but the rate of sustained virological response remains to low, not at least due to emergence of resistant virus strains. Less is known on HBV infection in children despite the extremely high rate of chronicity.</p> <p>Objective, Design, Setting, and Patient</p> <p>The case of a nine years old male with a 6 year history of chronic HBV infection, of those 5 years with antiviral treatment is described.</p> <p>Interventions and Main Outcome Measure(s)</p> <p>Before our lab was consulted, the patient was unsuccessfully treated with interferon, an obscure drug named Hepon, which should activate antiviral immune response, and Lamivudine, the latter most likely becoming ineffective due to the mergence of resistant subpopulations (rtL180 M, rtV207 M, two strains with stop codons at position rt188 and rt198, rtM204V (YVDD), rtM204K (YKDD)). Replacement of Lamivudine by adefovir displayed no advantage despite the lack of resistance mutations, thus no decrease in viremia was observed under adefovir treatment.</p> <p>Results and Conclusions</p> <p>Novel mutations in the YMDD motif and its direct neighbourhood were observed, both being compatible with Lamivudine resistance. No mutations were found that are associated with ADF resistance. Both, the clinical course of treatment and the genotypic resistance profile emphasize the need for systematic analyses of the HBV resistance mechanisms and structured therapy concept also for children chronically infected with HBV.</p

Processes to manage analyses and publications in a phase III multicenter randomized clinical trial

Background: The timely publication of findings in peer-reviewed journals is a primary goal of clinical research. In clinical trials, the processes leading to publication can be complex from choice and prioritization of analytic topics through to journal submission and revisions. As little literature exists on the publication process for multicenter trials, we describe the development, implementation, and effectiveness of such a process in a multicenter trial. Methods: The Hepatitis C Antiviral Long-Term Treatment against Cirrhosis (HALT-C) trial included a data coordinating center (DCC) and clinical centers that recruited and followed more than 1,000 patients. Publication guidelines were approved by the steering committee, and the publications committee monitored the publication process from selection of topics to publication. Results: A total of 73 manuscripts were published in 23 peer-reviewed journals. When manuscripts were closely tracked, the median time for analyses and drafting of manuscripts was 8 months. The median time for data analyses was 5 months and the median time for manuscript drafting was 3 months. The median time for publications committee review, submission, and journal acceptance was 7 months, and the median time from analytic start to journal acceptance was 18 months. Conclusions: Effective publication guidelines must be comprehensive, implemented early in a trial, and require active management by study investigators. Successful collaboration, such as in the HALT-C trial, can serve as a model for others involved in multidisciplinary and multicenter research programs. Trial registration The HALT-C Trial was registered with clinicaltrials.gov (NCT00006164)

Prevalence and clinical correlates of YMDD variants during lamivudine therapy for patients with chronic hepatitis B

YMDD variants of hepatitis B virus (HBV) emerge in some patients with chronic hepatitis B who receive lamivudine. YMDD variants were examined in 794 patients in 4 controlled studies of 1 year's duration. The long-term effects of YMDD variants were examined in a subset of patients treated up to 4 years. YMDD variants were detected by polymerase chain reaction (PCR) and restriction fragment-length polymorphism assays. After 1 year, YMDD variants were detected in 81 (24%) of 335 patients. In these patients, the median serum HBV DNA concentration at 1 year was <20% of the baseline level, and serum alanine transaminase (ALT) levels and liver histologic findings had significantly improved. In patients with YMDD variants who were treated for up to 4 years, median HBV DNA and ALT levels showed improvements. Sex, baseline body mass index, and HBV DNA level were associated with emergence of YMDD variants. Patients with YMDD variants losing clinical response with a significant increase in the HBV DNA and ALT levels may require additional therapy.published_or_final_versio

Serum Vitamin D Levels Are Not Predictive of the Progression of Chronic Liver Disease in Hepatitis C Patients with Advanced Fibrosis

In animal models and human cross-sectional studies, vitamin D deficiency has been associated with liver disease progression. Vitamin D supplementation has been suggested as a treatment to prevent disease progression. We sought to evaluate the role of vitamin D levels in predicting chronic liver disease development. We conducted a nested case-control study of vitamin D levels in subjects with (cases) and without (controls) liver histologic progression or clinical decompensation over the course of the HALT-C Trial. Vitamin D levels were measured at 4 points over 45 months. 129 cases and 129 aged-matched controls were included. No difference in baseline vitamin D levels were found between cases and controls. (44.8 ng/mL vs. 44.0 ng/mL, P = 0.74). Vitamin D levels declined in cases and controls over time (P = 0.0005), however, there was no difference in the level of decline (P = 0.37). Among study subjects with diabetes mellitius, baseline vitamin D levels were higher in cases, 49.9 ng/mL, than controls, 36.3 ng/mL. (P = 0.03) In addition, baseline vitamin D levels were higher in black case subjects, 32.7 ng/mL, than in black control subjects, 25.2 ng/mL (P = 0.08) No difference in vitamin D levels was found between patients with and without progression of hepatitis C-associated liver disease over 4 years. Our data do not suggest any role for vitamin D supplementation in patients with advanced chronic hepatitis C and raise the possibility that higher vitamin D levels may be associated with disease progression

Aplastic anemia and hepatitis C: Molecular biology exonerates another suspect

Objective. – To test the hypothesis that the rare, often fatal, syndrome of hepatitis-associated aplasia is associated with hepatitis C virus infection. Design. – Case series. Setting.-Tertiary referral centers in the United States, Japan, Italy, and Germany. Patients. – Twenty-eight patients with onset of aplastic anemia within 90 days after seeking medical attention for jaundice, or having serum transaminase levels 150% or more of normal (hepatitis-associated aplasia patients) and three patients who developed aplastic anemia following liver transplantation for non-A, non-B, hepatitis. Outcome Measures. - Presence of hepatitis C in serum, bone marrow, and liver samples, detected by the polymerase chain reaction; antibody testing; and percentage of activated peripheral cytotoxic T lymphocytes determined by immunophenotyping. Results. – Hepatitis ribonucleic acid was present in the serum samples of 10 (36%) patients with hepatitis-associated aplasia. However, hepatitic C virus viremia was associated with transfusions received after the onset of aplasia: seven (58%) of 12 patients with hepatitis-associated aplasia who had received 21 or more units of blood products at the time of serum sampling were viremic, compared with only three (19%) of 16 patients with hepatitis-associated aplasia who had received 20 or less units of blood products ( P <.05). Hepatitis C virus was not found in blood and bone marrow samples of three National Institutes of Health case patients tested at the time of diagnosis. None of three livers from non-A, non-B hepatitis patients who developed aplastic anemia after liver transplantation contained hepatitis C virus ribonucleic acid. Activated CD8 + T lymphocytes were elevated three- to 20-fold early in the course of hepatitis-associated aplasia. Conclusions. – Our results implicate a novel, non-A, non-B, and non-C agent in both hepatitis-associated aplasia and fulminant hepatitis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/38390/1/1840170227_ftp.pd