Are medical students being taught anatomy in a way that best prepares them to be a physician?

Reasoning in a clinical context is an attribute of medical expertise. Clinical reasoning in medical school can be encouraged by teaching basic science with a clinical emphasis. The aim of this study was to investigate whether anatomy is being taught in a way that facilitates the development of clinical reasoning. Two multiple-choice tests on thoracic anatomy were developed using a modified Delphi approach with groups of four clinical consultants and four teachers, respectively, expressing their opinions about knowledge relevant to thoracic anatomy. Validity was assessed by administering the tests to clinical consultants, anatomy teachers, and pre-course medical students. Post-course medical students took both tests to explore the focus of the course, i.e., whether it facilitated clinical reasoning. The pre-course students scored significantly lower than the teachers and post-course students on both tests and lower than the consultants on the consultants' test (P < 0.001 for all comparisons). The teachers significantly outperformed the consultants (P = 0.03 on the consultants' test, P < 0.001 on the teachers' test) and the medical students (P < 0.001 on both tests). The post-course students scored significantly lower on the consultants' test (P = 0.001) and significantly higher on the teachers' test (P = 0.02) than the consultants. This study demonstrates poor performances by medical students on a test containing clinically relevant anatomy, implying that the teaching they have received has not encouraged clinical reasoning.

Polymorphonuclear leukocytes restrict growth of Pseudomonas aeruginosa in the lungs of cystic fibrosis patients.

Cystic fibrosis (CF) patients have increased susceptibility to chronic lung infections by Pseudomonas aeruginosa, but the ecophysiology within the CF lung during infections is poorly understood. The aim of this study was to elucidate the in vivo growth physiology of P. aeruginosa within lungs of chronically infected CF patients. A novel, quantitative peptide nucleic acid (PNA) fluorescence in situ hybridization (PNA-FISH)-based method was used to estimate the in vivo growth rates of P. aeruginosa directly in lung tissue samples from CF patients and the growth rates of P. aeruginosa in infected lungs in a mouse model. The growth rate of P. aeruginosa within CF lungs did not correlate with the dimensions of bacterial aggregates but showed an inverse correlation to the concentration of polymorphonuclear leukocytes (PMNs) surrounding the bacteria. A growth-limiting effect on P. aeruginosa by PMNs was also observed in vitro, where this limitation was alleviated in the presence of the alternative electron acceptor nitrate. The finding that P. aeruginosa growth patterns correlate with the number of surrounding PMNs points to a bacteriostatic effect by PMNs via their strong O2 consumption, which slows the growth of P. aeruginosa in infected CF lungs. In support of this, the growth of P. aeruginosa was significantly higher in the respiratory airways than in the conducting airways of mice. These results indicate a complex host-pathogen interaction in chronic P. aeruginosa infection of the CF lung whereby PMNs slow the growth of the bacteria and render them less susceptible to antibiotic treatment while enabling them to persist by anaerobic respiration.

JNK1, but not JNK2, is required in two mechanistically distinct models of inflammatory arthritis.

The roles of the c-Jun N-terminal kinases (JNKs) in inflammatory arthritis have been investigated; however, the roles of each isotype (ie, JNK1 and JNK2) in rheumatoid arthritis and conclusions about whether inhibition of one or both is necessary for amelioration of disease are unclear. By using JNK1- or JNK2-deficient mice in the collagen-induced arthritis and the KRN T-cell receptor transgenic mouse on C57BL/6 nonobese diabetic (K/BxN) serum transfer arthritis models, we demonstrate that JNK1 deficiency results in protection from arthritis, as judged by clinical score and histological evaluation in both models of inflammatory arthritis. In contrast, abrogation of JNK2 exacerbates disease. In collagen-induced arthritis, the distinct roles of the JNK isotypes can, at least in part, be explained by altered regulation of CD86 expression in JNK1- or JNK2-deficient macrophages in response to microbial products, thereby affecting T-cell-mediated immunity. The protection from K/BxN serum-induced arthritis in Jnk1(-/-) mice can also be explained by inept macrophage function because adoptive transfer of wild-type macrophages to Jnk1(-/-) mice restored disease susceptibility. Thus, our results provide a possible explanation for the modest therapeutic effects of broad JNK inhibitors and suggest that future therapies should selectively target the JNK1 isoform.