Adverse learning strategy: the Adelaide Diagnostic Learning Inventory and its subscale replicability in a medical student population

The Adelaide Diagnostic Learning Inventory (ADLIMS) is a measure of learning styles and learning pathologies that was designed to investigate the impact of traditional approaches to learning versus problem-based learning and to identify students whose approach to learning tasks predicted poor academic performance. In this study, some important psychometric properties of the ADLIMS were examined, including its factor structure. In this study, factor replicability across samples was argued to provide a more robust and psychologically meaningful factor solution than that which can be obtained using traditional mathematical criteria. The results of the factor analysis did not confirm the presence of the four factor solution earlier reported for the ADLIMS, but did identify three clear factors that had very high replicability. An inspection of the items comprising these three factors showed that factor 1 tapped subjective distress related to poor study habits, lack of motivation to study, and distraction from social activities. Factor 2 tapped distress arising from high achievement expectations that were hampered by superficial or disorganized study habits that did not enable the student to grasp the relationships between concepts and ideas. Factor 3 tapped positive feelings and a sense of satisfaction associated with a problem-based approach to the learning of new study material. Although the internal reliability of the ADLIMS subscales met the requirements of a measure to be used in general research such as in the investigation of correlates among groups of medical students, they did not meet the higher requirements of a measure to be used to identify or predict individuals with pathological learning styles.     

PREVALENCE OF SELF-REPORTED DEPRESSION IN PATIENTS WITH RHEUMATOID ARTHRITIS

The prevalence of self-reported depressive symptoms was investigatedin a case-control study of patients with rheumatoid arthritis(RA) attending an out-patient clinic at the Middlesex Hospital.Patients selected their own controls, matched for age and sex.Previous attempts to measure depressive symptoms in RA havesuffered from measurement error due to criterion contamination,where psychological symptoms augment depressive scores. A totalof 163 patients (77% of the sample) and 115 matched pairs completedthe Hospital Anxiety and Depression Scale (HADS). The resultsIndicated that RA patients are more depressed and anxious thancontrols. The prevalence of depression above the cut-point was15%. This figure is comparable to other reports adjusted forcriterion contamination, but is lower than that of other studieswhich employ ‘contaminated’ tools. The depressionscale of the HADS appeared to be relatively free of criterioncontamination. Subject to further reliability testing, the HADSmay be a practical screening tool for practitioners to assesspatients in need of psychological interventions. KEY WORDS: Depression, Rheumatoid arthritis, Criterion contamination     

Studies on the histamine content of blood,with special reference to leukemia,leukemoid reactions and leukocytoses

The literature concerning blood histamine has been reviewed, including theevidence that the incorporation of histamine within the myeloid leukocytes maybe one of the metabolic functions of myelopoiesis. Data are presented on the histamine content of blood in normal subjects and in subjects with acute leukemia,chronic myelocytic leukemia, erythremia, and with leukocytoses or leukemoidreactions of other etiologies. The changing relationships of total blood histamineto unit myeloid cell histamine in subjects receiving irradiation therapy for chronicmyelocytic leukemia are also presented.

The data indicate that total blood histamine in chronic myelocytic leukemiais usually very high in comparison to normal, that the values in erythremia showa definite but less marked tendency in the same direction, while the values inleukocytoses of other etiology are, with few exceptions, normal or low. The bloodhistamine per million myeloid cells is, on the average, about twice normal in subjects with chronic myelocytic leukemia, within the normal range or a little lowin erythremia, and very low on the average in the group of leukocytoses studied.The suggestion is tentatively made that an aberration in this metabolic process(histamine incorporation within myeloid leukocytes) may be an inherent component of chronic myelocytic leukemia, whereas in physiologic leukocytoses andleukemoid reactions this is not the case.

Note: ACKNOWLEDGMENTSThe authors wish to express their grateful appreciation to Mr. John Fuschetti for valuable technicalassistance in performing the histamine determinations. The cooperation and aid of Dr. Gurth E. Carpenter, Dr. Henry H. Henstell, Dr. Myron Prinzmetal and of many members of the staff of WadsworthGeneral Hospital, Veterans Administration, Los Angeles were invaluable in obtaining blood specimensfrom suitable clinical material, and to them the authors wish to express their sincere thanks.

     

Site potential for challenge attrition in mice, rats and guinea pigs vaccinated with irradiated cercariae of Schistosoma mansoni

The potential sites of attrition of a challenge population of schistosomes have been investigated in mice, rats and guinea pigs vaccinated with irradiated cercariae of Schistosoma mansoni, by the use of challenge regimens that permit sequential site elimination. Vaccinated mice showed significant immunity to a percutaneous cercarial challenge, but were only marginally resistant to an i.v. challenge with healthy lung stage worms. Vaccinated rats and guinea pigs differed from mice, in that they were able to mediate significant challenge attrition at post-skin sites. Healthy lung worms were subject to immune elimination by rats in the lungs, or perhaps en route to the liver, but not in the liver itself. In contrast, guinea pigs had the capacity to kill challenge lung worms injected into either the lungs or the liver. Interestingly, lung worms harvested by extended incubation were shown to be sub-optimal in terms of viability, since they were eliminated in significant numbers when injected i.v. into vaccinated mice. These data show that different hosts vaccinated in essentially the same manner differ in terms of their site potential for challenge attrition. It is emphasised however, that sites implicated by these experiments as having the capacity to mediate immune elimination are not necessarily the sites at which challenge attrition occurs under normal circumstances.     

LATE ONSET HUNTINGTON'S DISEASE AS A CAUSE OF DEMENTIA: WHERE SHOULD THE CLINICIAN'S INDEX OF SUSPICION LIE?

Our experience with two genetically confirmed cases of late onset Huntington's disease (HD) in a longitudinal dementia research study suggested that clinical misdiagnosis can easily occur. We therefore undertook genetic testing for HD in a further 84 elderly subjects, 81 of whom had come to postmortem; 75 subjects had dementia and nine were normal controls. A quarter of the demented group had demonstrated extrapyramidal symptoms in life but in none had HD formed part of the differential diagnosis. Although no genetically confirmed cases were found in this second group, the original cases serve as a reminder that late onset HD is a cause of dementia. Genetic confirmation should be sought when the condition forms part of the final differential diagnosis. Further studies conducted in the routine clinical setting are now required since it is in this environment that late onset HD is likely to be misdiagnosed in favour of other forms of dementia.     

GPVI and integrin αIIbβ3 signaling in platelets

This review summarizes recent developments in our understanding of the molecular basis of platelet activation by two distinct types of surface receptor, the immunoglobulin GPVI, and the integrin alphaIIb beta3 (also known as GPIIbIIIa). These two classes of receptor signal through similar yet distinct tyrosine kinase-based signaling cascades leading to activation of phospholipase C gamma2. The significance of these signaling cascades in platelet adhesion and platelet aggregation at arterial rates of shear is discussed.     

A major role for Scar/WAVE-1 downstream of GPVI in platelets

BACKGROUND: The small GTPase Rac1 plays a critical role in lamellipodia assembly in platelets on matrix proteins in the absence or presence of G protein-coupled receptor (GPCR) agonists. Rac mediates actin assembly via Scar/WAVE, a family of scaffolding proteins that direct actin reorganization by relaying signals from Rac to the Arp2/3 complex. OBJECTIVE: To evaluate the role of Scar/WAVE-1 in mediating platelet activation and cytoskeletal reorganization. METHODS AND RESULTS: Using specific antibodies, we demonstrate that murine platelets, like human platelets, express Scar/WAVE-1 and Scar/WAVE-2. Lamellipodia formation in Scar/WAVE-1(-/-) platelets is markedly inhibited on immobilized collagen-related peptide (CRP) and on laminin, both of which signal through the collagen receptor GPVI. In contrast, lamellipodia formation on collagen, which requires release of the GPCR agonists ADP and thromboxane A(2), is not altered. Immobilized fibrinogen supports limited formation of lamellipodia in murine platelets, which is not altered in Scar/WAVE-1(-/-) platelets. As with Rac1(-/-) platelets, Scar/WAVE-1(-/-) platelets exhibit a marked inhibition of aggregation in response to CRP, whereas the response to the GPCR agonist thrombin is not altered. Platelet aggregation on immobilized collagen under shear, which is dependent on signaling by matrix and GPCR agonists, was unaltered in the absence of Scar/WAVE-1. CONCLUSION: This study demonstrates a major role for Scar/WAVE-1 in mediating platelet cytoskeletal reorganization and aggregate formation downstream of activation by GPVI but not by GPCR agonists.     

Identification and characterization of a DR4-restricted T cell epitope within chlamydia heat shock protein 60

An epitope within the 60 kD Chlamydia trachomatis heat shock protein (hsp) 60, recognized by a HLA-DRB1*0401-restricted T cell clone from a reactive arthritis patient, has been characterized. Stimulatory peptides contained a nine amino acid sequence (residues 38–46) predicted by algorithm to confer strong binding to DRB1*0401, with valine in the P1 position. The overall length of the peptide was critical for efficient recognition; peptides with at least one residue N-terminal to the putative P1 position were markedly more stimulatory than a peptide whose N-terminal is the P1 valine. Optimal responses were seen with 14mer peptides having two to three amino acids N- and C-terminal to the core 9mer. The sequence of the defined epitope is identical in hsp60 from both C. trachomatis and C. pneumoniae. Since the latter is a common respiratory pathogen, patients infected with C. trachomatis may already be primed for responses to hsp60 by prior infection with C. pneumoniae. Such secondary responses are important in the pathogenesis of chlamydia-induced inflammatory diseases such as trachoma. Priming by infection with enteric organisms was considered because of the similarity of the epitope sequence in Escherichia coli hsp60. However, although an E. coli-related peptide was recognized, intact E. coli hsp60 was not, suggesting that the epitope is cryptic in E. coli hsp60. Human hsp60 has six amino acid differences from chlamydial hsp60 in the epitope sequence and was not recognized. Thus cross-reactive recognition of self hsp60 could not be implicated in the pathogenesis of chlamydia-induced reactive arthritis in this patient.