BS15PFACILITATING NATIONAL CONSISTENCY IN BREAST CANCER DATA COLLECTION

In Australia there is currently no consistent approach to collecting breast cancer specific data. The National Health Data Dictionary (NHDD) recommends a core set of generic data items for clinical cancer registration. However this list does not include the more detailed items required by specific tumour streams. The NBCC has developed a supplementary set of Breast Specific Data Items and definitions to serve as a guide for specialist breast cancer data collection in Australia. A multidisciplinary Working Group comprising clinical and consumer representation, including three breast surgeons, identified 16 breast specific data items for collection. The items are designed to align with items collected through the RACS National Breast Cancer Audit and leading cancer centres. A range of items from patient data (menopausal status), diagnostic data (HER2 status, sentinel lymph node), treatment (surgical margin clearance and involvement), and breast reconstruction are included. The data items are recommended as best practice for breast cancer specific data collection and aim to facilitate national consistency in defining, recording, and monitoring information about patients with breast cancer. This national approach will contribute to improved patient outcomes by informing planning, quality improvement and evaluation strategies for cancer services. The items are currently being piloted in two sites in NSW and will be available nationally in late 2007.     

Understanding the minimum clinically important difference: a review of concepts and methods.

BACKGROUND CONTEXT: The effectiveness of spinal surgery as a treatment option is currently evaluated through the assessment of patient-reported outcomes (PROs). The minimum clinically important difference (MCID) represents the smallest improvement considered worthwhile by a patient. The concept of an MCID is offered as the new standard for determining effectiveness of a given treatment and describing patient satisfaction in reference to that treatment. PURPOSE: Our goal is to review the various definitions of MCID and the methods available to determine MCID. STUDY DESIGN: The primary means of determining the MCID for a specific treatment are divided into anchor-based and distribution-based methods. Each method is further subdivided and examined in detail. METHODS: The overall limitations of the MCID concept are first identified. The basic assumptions, statistical biases, and shortcomings of each method are examined in detail. RESULTS: Each method of determining the MCID has specific shortcomings. Three general limitations in the accurate determination of an MCID have been identified: the multiplicity of MCID determinations, the loss of the patient's perspective, and the relationship between pretreatment baseline and posttreatment change scores. CONCLUSIONS: An ideal means of determining the MCID for a given intervention is yet to be determined. It is possible to develop a useful method provided that the assumptions and methodology are initially declared. Our efforts toward the establishment of a MCID will rely on the establishment of specific external criteria based on the symptoms of the patient and treatment intervention being evaluated.     

Oxford Handbook of Pre-hospital Care

There are at least two reasons why this Oxford handbook meritsa review in the British Journal of Anaesthesia. A proportionof readers will be involved at some time during their careerin the provision of pre-hospital care and most of us will onoccasion manage patients on their arrival in hospital followingcare for acute medical and surgical problems in the community.The Oxford series aims to act as a succinct primer in each subject,and this one succeeds. The contents page illustrates its     

Association of ex-vivo expanded human mesenchymal stem cells and rhBMP-7 is highly effective in treating critical femoral defect in rats

Mesenchymal stem cells (MSC), easily culture-expanded from bone marrow, can significantly enhance bone defect healing. Several proteins, such as the bone morphogenetic proteins (BMPs) and in particular BMP-7, are involved in bone formation in vitro and in vivo. In this preclinical study, we evaluated if the association of human MSC (hMSC) with BMP-7 had synergic action on bone healing. Rat femoral defects (n=12) were treated with: autoclaved bone and mononucleated cells (MNC) as control group G1; bone and hMSC, group G2; bone with BMP-7, group G3; bone and hMSC plus BMP-7, group G4. Defect regeneration was evaluated with plain radiographs after 2, 4, 8 and 12 weeks and with histological analysis. We observed organized trabeculae bridging between the osteotomic ends of the host bone in rats treated with the association of hMSC and rhBMP-7. These trabeculae, formed by a core of devitalized tissue surrounded by osteoblasts, osteocytes and osteoclasts, were continuous with a cortical-like structure of bony tissue. Such new bone formation of the group treated with the association of hMSC and rhBMP-7 (G4) was clearly superior compared to rats treated with rhBMP-7 (G2) or hMSC (G3) alone, as shown by radiographic analysis and histological study. The present study suggests that the association of hMSC and BMP-7 is more effective than hMSC or BMP-7 alone in the healing of femoral defects in rats. Further studies with larger samples are required to confirm these results and to evaluate the best dosage.     

Fluoridated elastomers: effect on the microbiology of plaque.

The objective of this study was to investigate the effect of fluoridated elastomeric ligatures on the microbiology of local dental plaque in vivo. This randomized, prospective, longitudinal, clinical trial had a split-mouth crossover design. The subjects were 30 patients at the beginning of their treatment with fixed orthodontic appliances in the orthodontic departments of the Liverpool and the Sheffield dental hospitals in the United Kingdom. The study consisted of 2 experimental periods of 6 weeks with a washout period between. Fluoridated elastomers were randomly allocated at the first visit to be placed around brackets on tooth numbers 12, 11, 33 or 22, 21, 43. Nonfluoridated elastomers were placed on the contralateral teeth. Standard nonantibacterial fluoridated toothpaste and mouthwash were supplied. After 6 weeks (visit 2), the elastomers were removed, placed in transport media, and plated on agar within 2 hours. Nonfluoridated elastomers were placed on all brackets for 1 visit to allow for a washout period. At visit 3, fluoridated elastomers were placed on the teeth contralateral to those that received them at visit 1. At visit 4, the procedures at visit 2 were repeated. Samples were collected on visits 2 and 4. A logistic regression was performed, with the presence or absence of streptococcal or anaerobic growth as the dependent variable. A mixed-effects analysis of variance was carried out with the percentage of streptococcal or anaerobic bacterial count as the dependent variable. The only significant independent variables were the subject variable (P =<.001) for the percentage of streptococcal and anaerobic bacterial count and the visit variable for the percentage of streptococcal count (P =<.001). The use of fluoridated or nonfluoridated elastomers was not significant for percentage of either streptococcal (P =.288) or anaerobic count (P =.230). Fluoridated elastomers are not effective at reducing local streptococcal or anaerobic bacterial growth after a clinically relevant time in the mouth.     

Diabetes mellitus, hypertension and medial temporal lobe atrophy: the LADIS study.

HYPOTHESIS: Based on recent findings on the association between vascular risk factors and hippocampal atrophy, we hypothesized that hypertension and diabetes mellitus (DM) are associated with medial temporal lobe atrophy (MTA) in subjects without disability, independent of the severity of white matter hyperintensities. METHODS: In the Leukoaraiosis And DISability in the elderly (LADIS) study, we investigated the relationships between DM, hypertension, blood pressure and MTA in 582 subjects, stratified by white matter hyperintensity severity, using multinomial logistic regression. MTA was visually scored for the left and right medial temporal lobe (score 0-4), and meaned. RESULTS: Mean age was 73.5 years (sd 5.1), 54% was female. Of the subjects, 15% had DM, and 70% had a history of hypertension. The likelihood of having MTA score 3 was significantly higher in subjects with DM (OR 2.9; 95% CI: 1.1-7.8) compared with an MTA score of 0 (no atrophy). The odds ratio for MTA score 2 was not significantly increased (OR 1.8; CI: 0.9-4). Systolic and diastolic blood pressure and a history of hypertension were not associated with MTA. There was no interaction between DM and hypertension. Stratification on white matter hyperintensities (WMH) did not alter the associations. CONCLUSION: Our study strengthens the observation that MTA is associated with DM, independently of the amount of small vessel disease as reflected by WMH.     

Histamine and tryptase modulate asthmatic airway smooth muscle GM-CSF and RANTES release.

Degranulating mast cells are increased in the airway smooth muscle (ASM) of asthmatics, where they may influence ASM function. The aim of the present study was to determine whether histamine and tryptase modulate ASM cell granulocyte-macrophage colony-stimulating factor (GM-CSF) and RANTES (regulated on activation, normal T-cell expressed and secreted) release and also to examine which receptors are involved in this release. Confluent, quiescent ASM cells from asthmatic and nonasthmatic donors were treated with histamine (1 microM-100 microM) with and without histamine receptor antagonist pre-treatment, or the protease-activated receptor (PAR)-2 agonists tryptase (0.5-5 nM) and SLIGKV (100 and 400 microM). The cells were then stimulated with interleukin (IL)-1beta and/or tumour necrosis factor (TNF)-alpha (10 ng.mL(-1)) or left unstimulated for 24 h. Release of GM-CSF and RANTES was determined by ELISA and prostaglandin (PG)E(2) measured by enzyme immunoassay. Neither histamine nor tryptase induced ASM GM-CSF or RANTES secretion. However, histamine increased IL-1beta-induced GM-CSF release and markedly reduced TNF-alpha-induced RANTES release by both asthmatic and nonasthmatic cells to a similar extent, but did not modulate PGE(2) release. All changes involved activation of the histamine H1 receptor as they were partially or fully blocked by chlorpheniramine, but not ranitidine. Tryptase, via its proteolytic activity, also potentiated GM-CSF, but not RANTES, release from asthmatic and nonasthmatic ASM cells induced by both cytokines. PAR-2 involvement in the tryptase potentiation was unlikely because SLIGKV had no effect. In conclusion, mast cells, through histamine and tryptase, may locally modulate airway smooth muscle-induced inflammation in asthma.