Resection arthroplasty of the infected shoulder: a salvage procedure for the elderly patient

Infection of the shoulder joint is a challenging problem for the orthopaedic surgeon. Several treatment options have been proposed. Here, we evaluate the results achieved following resection arthroplasty of the shoulder in seven patients. We performed resection arthroplasty in seven cases to treat a chronic uncontrollable infection of the shoulder. Three patients had an infected shoulder arthroplasty, one had an infected non-united arthrodesis, one was treated for an infected osteosynthesis, one had an infected rotator cuff repair and one patient had a septic arthritis of the shoulder joint. All patients were reviewed after a mean of 252 days. The functional outcome was evaluated using the Constant and DASH score. C-Reactive Protein levels were determined to evaluate the presence of residual infection. Except for one doubtful result, all our patients remained free of infection and there was excellent pain relief after the resection. Nevertheless, the functional outcome was poor: the mean Constant score was 25.7 and the mean DASH score was 69.3. Resection arthroplasty of the shoulder is a valuable treatment option for infection of the shoulder, especially in older patients with a poor mental and physical condition who suffer intolerable pain.     

The deletion in both common types of hereditary persistence of fetal hemoglobin is approximately 105 kilobases

The most common forms of hereditary persistence of fetal hemoglobin (HPFH) involve large deletions that remove the adult delta and beta genes but leave the paired fetal genes (G gamma and A gamma) intact. The size of these deletions has previously eluded exact definition. Using pulsed-field gel electrophoresis and the enzyme SfiI, which cuts only rarely in genomic DNA, we have constructed a large-scale restriction map of the beta-globin cluster in normal and HPFH DNA. The deletions in HPFH-1, which occurs in American blacks, and in HPFH-2, which occurs in Ghanaian blacks, are found to be approximately 105 kilobases (kb) in length, though the endpoints are staggered by approximately 5 kb. The fact that two previously reported gamma delta beta-thalassemia deletions to the 5' side of the beta-globin cluster are also about 100 kb suggests a common mechanism, possibly involving the loss of a complete chromatin loop.     

The Apple 1 and Apple 4 domains of factor XI act synergistically to promote the surface-mediated activation of factor XI by factor XIIa

Binding sites for high molecular weight kininogen (HK) and for factor XIIa are present in the Apple 1 (A1) and the A4 domains of factor XI, respectively. To define the roles of these two sites in surface- mediated factor-XI activation we prepared conformationally constrained synthetic peptides and recombinant A1 domain (rA1) and determined their effects on the activation of factor XI by factor XIIa in the presence of HK and either kaolin or dextran sulfate. Surface-mediated factor-XI activation by factor XIIa was inhibited by a conformationally constrained A4 peptide (Ala317-Gly350), by an A1 peptide (Phe56-Ser86), and by rA1 (Glu1-Ser90). When used in combination at equimolar concentrations, rA1 and A4 peptide were 10-fold more effective than either one alone in inhibiting surface-mediated activation of factor XI by factor XIIa. The A4 peptide was a competitive inhibitor of factor XIIa amidolytic activity and a noncompetitive inhibitor of factor-XI activation by factor XIIa, whereas rA1 and the A1 peptide did not inhibit factor XIIa. The rA1 domain inhibited factor XI binding to HK, whereas the A4 peptide did not. We conclude that specific sequences exposed on the surfaces of the A1 (Val59-Lys83) and A4 (Ala317-Gly350) domains of factor XI act synergistically to promote surface-mediated factor-XI activation by factor XIIa in the presence of HK by binding factor XI to surface-bound HK (A1 domain) and by binding factor XIIa near the cleavage site (Arg369-Ile370) of factor XI (A4 domain).     

Nonrandom inactivation of the X chromosome in early lineage hematopoietic cells in carriers of Wiskott-Aldrich syndrome

The Wiskott-Aldrich syndrome (WAS) is an X-linked (Xp11.22) recessive immunodeficiency syndrome characterized by susceptibility to opportunistic and pyogenic infections, thrombocytopenia, and eczema. Previous studies of obligate carriers of WAS documented that nonrandom inactivation of the X chromosome carrying the defective gene is observed in all peripheral blood cells. The existence of both abnormal platelets and lymphocytes is consistent with a defect that affects early hematopoietic precursors. We isolated CD34+ hematopoietic progenitor cells collected from obligate carriers of WAS by apheresis and used polymerase chain reaction analysis of a polymorphic variable number of repeats (VNTR) within the X-linked androgen receptor to document nonrandom inactivation. These data show that nonrandom inactivation of the X-chromosome in WAS-obligate carriers occurs early during hematopoietic differentiation.     

Routine oral examination: Clinical vignettes,a promising tool for continuing professional development?

Objectives

To develop content for an educational system for dental professionals to be used for patient-tailored evidence-based decisions regarding routine oral examinations (ROEs) and to test the model as a tool in dental education.

Methods

Initially, an electronic database was developed comprising conclusive data of a structured literature search and 27 ROE clinical cases which were selected on predefined criteria. A RAND-modified Delphi procedure was successfully conducted with 31 multidisciplinary dental experts. Twenty-one selected risk factors for oral disease were assessed for feasibility and subsequently modelled into 19 risk based clinical vignettes, each representing a specific group of ROE-patients. Each vignette comprised all relevant clinical and non-clinical data. Expert judgements were collected including ROE-content, risk level, bitewing frequency and recall interval. Feedback regarding evidence was provided for each of the topics. A pilot with 35 experienced General Dental Practitioners (GDPs) was conducted to assess the reliability of the model for continuing professional development (CPD). Decisions made on content screening items, bitewing frequencies and recall interval were compared with expert opinions.

Results

A comprehensive set of clinical vignettes was developed. Expert consensus was reached with regard to risk factors to be applied, content of ROE-items, bitewing frequency and recall interval. Differences between GDPs and experts were found especially concerning recall length in low-risk patient groups.

Conclusions

Clinical vignettes provide a promising educational instrument for CPD to improve clinical performance. Further research is needed to test the reliability of these set of 19 vignettes.