Influence of postal distribution of the Royal College of Radiologists' guidelines, together with feedback on radiological referral rates, on X-ray referrals from general practice: a randomized controlled trial.
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BACKGROUND: The Royal College of Radiologists (RCR) have produced regularly updated guidelines on radiological referrals since 1990. A small study in 1992 showed postal distribution of guidelines reduced general practitioners' referrals over the subsequent 9 weeks. However there have been no randomized trials of the longer term effects of radiological guidelines and feedback on referral rates on X-ray requests from primary care. OBJECTIVES: To see if the introduction of radiological guidelines into general practices together with feedback on referral rates reduces the number of GP radiological requests over one year; and to explore GPs'attitudes to the guidelines. METHODS: Sixty-nine practices referring patients to St George's Healthcare Trust were randomly allocated to intervention or control groups. In February 1995 a GP version of the RCR guidelines was sent to each GP in the 33 practices in the intervention group. After 9 months intervention, practices were sent revised guidelines with individual feedback on the number of examinations requested in the past 6 months. The total number of requests per practice was compared for the year before and the year after the introduction of the guidelines. Control practices were sent the guidelines at the end of the study. All doctors were sent a questionnaire about the guidelines. RESULTS: A total of 43 778 radiological requests were made during the two years 1994-1996. In practices receiving the guidelines there was a 20% reduction in requests for spinal examinations compared with control practices (P < 0.05). This corresponded to the effect reported by GPs. There was also a 10% difference between the groups in the total number of requests made, but due to wide interpractice variation in referral rates this failed to reach statistical significance. CONCLUSIONS: Introduction of radiological guidelines together with feedback on referral rates was effective in reducing the number of requests for spinal examinations over one year. Wider use of GP-orientated guidelines with regular updating and feedback might save costs and reduce unnecessary irradiation of patients. (+info)
Silent lacunar lesions detected by magnetic resonance imaging of children with brain tumors: a late sequela of therapy.
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BACKGROUND: Cerebral lacunes, which generally appear on magnetic resonance imaging as foci of white matter loss, usually occur in adults after ischemic infarcts. We report the development of lacunes in children after therapy for brain tumors. PATIENTS AND METHODS: We reviewed the clinical characteristics and radiologic studies of 524 consecutive children with brain tumors treated over a 10-year period. We documented the neuropsychologic findings associated with lacunes and the factors predictive of lacunar development. RESULTS: Lacunes developed in none of the 103 patients observed or treated with surgery alone. Twenty-five of the 421 patients treated with chemotherapy or radiation therapy or both had lacunes. Patients were a median of 4.5 years old at the time of both diagnosis (range, 0.3 to 19.8 years) and radiotherapy (range, 1.5 to 20 years). Fourteen patients were treated with craniospinal irradiation, and 11 were treated with local radiotherapy. The median time from radiotherapy to the appearance of lacunes was 2.01 years (range, 0.26 to 5.7 years). For all patients, lacunes were an incidental finding with no corresponding clinical deficits. The factor most predictive of lacunar development was age less than 5 years at the time of radiotherapy (P =.010). There was no significant difference in estimated decline in intelligence quotient scores between patients with lacunes and age and diagnosis-matched controls. CONCLUSION: Lacunes may be caused by therapy-induced vasculopathy in children with brain tumors, with the most significant predictor being age less than 5 years at the time of radiotherapy. (+info)
A genetic risk factor for mouse neural tube defects: defining the embryonic basis.
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Genetic polymorphisms are thought to play an important role in determining susceptibility to neural tube defects (NTDs), for example between different ethnic groups, but the embryonic manifestation of these polymorphic genetic influences is unclear. We have used a mouse model to test experimentally whether polymorphic variations in the pattern of cranial neural tube closure can influence susceptibility to NTDs. The site at which cranial neural tube closure begins (so-called closure 2) is polymorphic between inbred mice. Strains with a caudal location of closure 2 (e.g. DBA/2) are relatively resistant to NTDs, whereas strains with a rostrally positioned closure 2 (e.g. NZW) exhibit increased susceptibility to NTDs. We tested experimentally whether altering the position of closure 2 can affect susceptibility to cranial NTDs, by back- crossing the splotch ( Sp (2H) ) mutant gene onto the DBA/2 background. As a control, Sp (2H) was transferred onto the NZW background, which resembles splotch mice in its closure pattern. Approximately 80% of Sp (2H) homozygotes develop NTDs, both cranial (exencephaly) and spinal (spina bifida). After transfer to the DBA/2 background, the frequency of cranial NTDs was reduced significantly in Sp (2H) homozygotes, confirming a protective effect of caudal closure 2. In contrast, Sp (2H) homozygotes on the NZW background had a persistently high frequency of cranial NTDs. The frequency of spina bifida was not altered in either backcross, emphasizing the specificity of this genetic effect for cranial neurulation. These findings demonstrate that variation in the pattern of cranial neural tube closure is a genetically determined factor influencing susceptibility to cranial NTDs. (+info)
Extensive glycosylation changes revealed by lectin histochemistry in morphologically normal prenatal tissues of the mouse mutant undulated (un/un).
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Recently we observed that in human embryos and fetuses with a variety of malformations, not only malformed tissues, but also several non-malformed tissues displayed alterations in the glycosylation pattern. It was the aim of this work to investigate this more or less inexplicable phenomenon under experimental conditions. To this end, we studied a well known mouse model, the mouse mutant undulated, which has an exactly defined genetic defect (substitution in the pax-1 gene) leading to a localized malformation in the vertebral column. The glycosylation pattern was studied using lectin histochemistry. Distribution of binding sites for the lectins RCA I, Con A, SNA, SBA, PNA, LTA and WGA was studied during the organogenesis stages (i.e., days 11-18). It was striking that in mutants, changes in the glycosylation pattern were found not only in the malformed organ (i.e., vertebral anlage), but also in other embryonic tissues, which showed normal morphology. This suggests that the altered glycosylation seems to be a part of genetically determined phenomena throughout the entire organism. Our results show that a defect in a gene with a very restricted expression can cause universal changes in the glycosylation pattern during development. (+info)
Platyspondyly and shortness of vertebral column in farmed Atlantic salmon Salmo salar in Norway--description and interpretation of pathologic changes.
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Body malformation due to shortness of the vertebral column, in most cases of unknown cause, has been observed in fish for more than 100 yr. It periodically occurs with high prevalence in farmed Atlantic salmon Salmo salar in Norway, and this paper describes the results of macroscopic, radiographic and histologic examination of parr and seawater-transferred fish. The vertebral bodies in both age groups did not acquire the length that they normally should due to a growth disturbance leading to the condition of platyspondyly and shortness in the column. The pathologic changes became visible at different ages in both groups and the process apparently starts in intervertebral tissues. There was proliferation of connective tissue and blood vessels, and sometimes infiltration with inflammatory cells, around affected vertebrae, especially in seawater-transferred fish. This is the first description of inflammation in abnormally short-spined fish, and it may indicate an infectious etiology, at least in farmed seawater-transferred salmon. (+info)
The branchial arches and HGF are growth-promoting and chemoattractant for cranial motor axons.
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During development, cranial motor neurons extend their axons along distinct pathways into the periphery. For example, branchiomotor axons extend dorsally to leave the hindbrain via large dorsal exit points. They then grow in association with sensory ganglia, to their targets, the muscles of the branchial arches. We have investigated the possibility that pathway tissues might secrete diffusible chemorepellents or chemoattractants that guide cranial motor axons, using co-cultures in collagen gels. We found that explants of dorsal neural tube or hindbrain roof plate chemorepelled cranial motor axons, while explants of cranial sensory ganglia were weakly chemoattractive. Explants of branchial arch mesenchyme were strongly growth-promoting and chemoattractive for cranial motor axons. Enhanced and oriented axon outgrowth was also elicited by beads loaded with Hepatocyte Growth Factor (HGF); antibodies to this protein largely blocked the outgrowth and orientation effects of the branchial arch on motor axons. HGF was expressed in the branchial arches, whilst Met, which encodes an HGF receptor, was expressed by subpopulations of cranial motor neurons. Mice with targetted disruptions of HGF or Met showed defects in the navigation of hypoglossal motor axons into the branchial region. Branchial arch tissue may thus act as a target-derived factor that guides motor axons during development. This influence is likely to be mediated partly by Hepatocyte Growth Factor, although a component of branchial arch-mediated growth promotion and chemoattraction was not blocked by anti-HGF antibodies. (+info)
Osteopenia and decreased bone formation in osteonectin-deficient mice.
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Bone continuously remodels in response to mechanical and physiological stresses, allowing vertebrates to renew bone as adults. Bone remodeling consists of the cycled synthesis and resorption of collagenous and noncollagenous extracellular matrix proteins, and an imbalance in this process can lead to disease states such as osteoporosis, or more rarely, osteopetrosis. There is evidence that the extracellular matrix glycoprotein osteonectin or secreted protein acidic and rich in cysteine (BM-40) may be important in bone remodeling. Osteonectin is abundant in bone and is expressed in areas of active remodeling outside the skeleton. In vitro studies indicate that osteonectin can bind collagen and regulate angiogenesis, metalloproteinase expression, cell proliferation, and cell-matrix interactions. In some osteopenic states, such as osteogenesis imperfecta and selected animal models for bone fragility, osteonectin expression is decreased. To determine the function of osteonectin in bone, we used contact x-ray, histomorphometry, and Northern blot analysis to characterize the skeletal phenotype of osteonectin-null mice. We found that osteonectin-null mice have decreased bone formation and decreased osteoblast and osteoclast surface and number, leading to decreased bone remodeling with a negative bone balance and causing profound osteopenia. These data indicate that osteonectin supports bone remodeling and the maintenance of bone mass in vertebrates. (+info)
Anterior surgical approaches to the sub-axial cervical spine.
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Anterior cervical spine surgery has come of age, as a golden route for treating anteriorly placed cervical compressions ranging from simple prolapsed disc to long segment pathologies like ossification of posterior longitudinal ligaments and cervical spondylotic myelopathy. Numerous technical modifications of the procedure are described. The role of stabilisation established for several pathologies, is still debateable in surgery for cervical disc. Bone is the ideal tissue for fusion. Hydroxyapetite implants are goods, but costly for our set up. Methylmethacrylate has a limited role in elderly patients with malignancy and a short life expectancy. Anterior cervical instrumentation has mushroomed over the last decade. Acceptable as methods of immediate stabilisation, the choice of the system varies with the surgeon. The authors use simple titanium plates with locking screws for the purpose. (+info)