Measuring professionalism in a physiatry residency training program

A 12-item questionnaire modeled after the one prepared by the American Board of Internal Medicine dealing with professionalism was distributed to 122 physiatry residents representing six training programs, of whom 59% (72) responded. The mean item score on the survey was 7.7 (SD = 1.0) on a scale from 1 to 10, where 10 represents the highest level of professionalism. The internal reliability of the questionnaire was found to be satisfactory (Cronbach's alpha = 0.75). A factor analysis of the questionnaire items resulted in three factors explaining 64% of the variance. These factors were: excellence, honor/integrity, and altruism/respect; Eigen values were 3.35, 2.37, and 1.31, respectively. These factors are similar to those obtained in the American Board of Internal Medicine survey. This similarity is a positive feature in ongoing efforts to develop a reliable tool for measuring professionalism in physiatry residency training.     

Acquisition versus retrieval deficits in traumatic brain injury: implications for memory rehabilitation

OBJECTIVE: To examine whether impaired memory in persons with traumatic brain injury (TBI) is caused by impaired initial acquisition or compromised retrieval from long-term storage. DESIGN: Prospective matched controlled trial. SETTING: Postacute rehabilitation institute. PARTICIPANTS: Patients with moderate to severe TBI (n = 28) and 21 matched, healthy controls (HCs). MAIN OUTCOME MEASURES: Patients with TBI and HC subjects were equated on initial acquisition on a verbal list-learning task. Recall and recognition performance was then evaluated at 30- and 90-minutes after learning. RESULTS: All HC subjects and 20 subjects with TBI (TBI-MET) were able to meet the learning criterion, but the TBI-MET group took significantly more trials than HC subjects to do so. However, after equating groups on acquisition, the TBI-MET group did not differ from controls on recall and recognition at both the 30- and 90-minute delays. Eight TBI subjects showed severe learning deficits (TBI-NOT MET) because they never learned the task, and showed significantly impaired recall and recognition performance. The 2 TBI groups did not differ on measures of severity of injury, but the TBI-NOT MET group performed significantly below the TBI-MET group on executive functioning. Rate of forgetting did not differ across the 3 groups. CONCLUSIONS: Results suggest that memory impairment after TBI is caused primarily by deficiencies in initial acquisition of verbal information rather than in compromised retrieval. The findings have significant implications for the rehabilitation and treatment of individuals with TBI.     

Post-operative blood salvage and retransfusion in total hip and knee arthroplasty

This retrospective study evaluated the safety and efficacy of post-operative blood salvage and retransfusion in 430 patients undergoing total hip arthroplasty and 530 patients undergoing total knee arthroplasty. Volumes of autologous blood retransfused (mean +/- SD) were 525 +/- 75 and 660 +/- 95 ml in the hip and knee replacement groups, respectively. Overall, 230 patients (24%) also required allogeneic blood transfusion. In a subgroup of 150 randomly selected patients, the values of free haemoglobin in the allogeneic, autologous and patients' blood at the time of surgery were 0.568 +/- 0.112, 0.272 +/- 0.067 and 0.032 +/- 0.011 g/l, respectively. On the first and third post-operative days, the levels in patients' blood were 0.092 +/- 0.039 and 0.057 +/- 0.028 g/l, respectively. There were no major complications; transient chills and fever were reported in 99 (10.3%) and 115 patients (12.0%), respectively. In conclusion, post-operative blood salvage and retransfusion is a safe way to reduce the need for allogeneic blood transfusion in patients undergoing elective orthopaedic surgery.     

B lymphoblastoid cell lines with normal and defective O-glycosylation established from an individual with blood group Tn

Individuals with the Tn blood group contain terminal serine/threonine- linked N-acetylgalactosamine residues in their blood cells. This is due to lack of UDP-D-galactose: D-N-acetyl galactosamine beta-D-galactosyl transferase from part of their red cells and probably from their leukocytes. We have established B lymphoblastoid cell lines from such an individual by in vitro infection of his lymphocytes with Epstein- Barr virus. The original line contained a mixture of cells reactive and nonreactive with Helix pomatia lectin (Hp). These cells were subcloned after staining with fluorescent Hp by a fluorescence-activated cell sorter (FACS) into homogeneous, phenotypically stable lines of Hp- positive (Hp+) and Hp-negative (Hp-) cells. The molecular differences between the membrane glycoproteins were characterized by carbohydrate- specific surface labeling techniques, Hp affinity chromatography, polyacrylamide slab gel electrophoresis and glycopeptide/oligosaccharide analysis. The major O-glycosidic membrane glycoprotein (GP105) was retained on Hp-Sepharose columns only from Hp+ cells, whereas the common leukocyte antigen (GP160-200) was partially retained on Hp columns from both lines. These proteins were isolated by immune precipitation with monoclonal antibodies and characterized. The results show that the GP105 glycoprotein from Hp+ cells contains terminal N-acetylgalactosamine residues but also more complex oligosaccharides. The common leukocyte antigen showed different electrophoretic mobilities in Hp+ and Hp- cells. UDP-galactose D-N- acetyl galactosamine beta-galactosyl transferase was almost absent in the Hp+ cells. These cell lines are useful for studies on the functional role and regulation of the biosynthesis of O-glycosidic carbohydrates.     

Evolution of the receptor binding properties of the influenza A(H3N2) hemagglutinin

The hemagglutinin (HA) of influenza A(H3N2) virus responsible for the 1968 influenza pandemic derived from an avian virus. On introduction into humans, its receptor binding properties had changed from a preference for avian receptors (α2,3-linked sialic acid) to a preference for human receptors (α2,6-linked sialic acid). By 2001, the avidity of human H3 viruses for avian receptors had declined, and since then the affinity for human receptors has also decreased significantly. These changes in receptor binding, which correlate with increased difficulties in virus propagation in vitro and in antigenic analysis, have been assessed by virus hemagglutination of erythrocytes from different species and quantified by measuring virus binding to receptor analogs using surface biolayer interferometry. Crystal structures of HA–receptor analog complexes formed with HAs from viruses isolated in 2004 and 2005 reveal significant differences in the conformation of the 220-loop of HA1, relative to the 1968 structure, resulting in altered interactions between the HA and the receptor analog that explain the changes in receptor affinity. Site-specific mutagenesis shows the HA1 Asp-225→Asn substitution to be the key determinant of the decreased receptor binding in viruses circulating since 2005. Our results indicate that the evolution of human influenza A(H3N2) viruses since 1968 has produced a virus with a low propensity to bind human receptor analogs, and this loss of avidity correlates with the marked reduction in A(H3N2) virus disease impact in the last 10 y.Surveillance of influenza viruses is essential for updating vaccines, for tracking the emergence of drug resistant viruses, and for monitoring zoonotic infections. It also gives important insights into the mechanisms of virus evolution. This is particularly the case for interpreting the correlation between antigenic differences and changes in the sialic acid receptor binding properties of the HA glycoprotein. The correlation in these two properties arises because of the close proximity on HA of binding sites for antibodies that neutralize virus infectivity and the sialic acid receptor binding pocket (1), and accounts for the observations that mutations that prevent antibody binding can also result in changes in receptor binding (2–7). Reduction in affinity of human H3N2 viruses for avian receptors since the beginning of the pandemic in 1968 has meant that by the 1990s viruses with reduced ability to agglutinate chicken erythrocytes had emerged (8, 9). Moreover, viruses isolated after 1999 were shown to have reduced affinity for both human and avian receptors, a feature that correlated with their poor growth properties in eggs and different cells in culture (9–14). The evolution of the HA has resulted in at least three key changes that influence receptor binding. Two sequential substitutions occurred at residue 225: in 2001–2002, a substitution Gly-225→Asp was accompanied by a Trp-222→Arg substitution, and in 2004–2005, an Asp-225→Asn substitution was accompanied by the substitution Ser-193→Phe (while maintaining arginine at position 222). Residue 226, a key amino acid in determining receptor specificity (15), also changed twice: before 2001, Leu-226→Val, and in 2004, Val-226→Ile (Fig. S1).To correlate these amino acid substitutions with the biological properties of the viruses, we have analyzed the receptor binding characteristics of H3N2 viruses isolated between 2001 and 2010, examined changes in their ability to infect cells in culture, and determined the structures of two HAs of virus isolates from 2004 and 2005 in the absence of receptor and complexed with a human receptor analog. The data show that the progressive decrease in binding of these viruses to human receptors from 2000 onward correlates with changes in the efficiencies of infection of cultured cells. Comparison of structural data for HAs of viruses from 1968, 2004, and 2005 explain how particular mutations that affect the conformation of the HA1 220-loop component of the receptor binding site define the receptor binding phenotype of recent H3N2 human influenza viruses.