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991.
OBJECTIVES: To determine the usefulness of electrocardiography (ECG) and chest radiography (CXR) in evaluation of patients referred to the pediatric cardiologist for the evaluation of heart murmur or chest pain. DESIGN: In this prospective study, 106 consecutive outpatients were categorized with no heart disease, possible heart disease, or definite heart disease based on history and physical examination; they then underwent ECG and CXR. Studies were reviewed and the examining cardiologist could change the diagnosis and order an echocardiogram. SETTING: Academic pediatric cardiology practice. RESULTS: In patients thought to have no heart disease, the diagnosis was changed to definite heart disease in four solely on the basis of abnormal CXR or ECG. In 25 patients thought to have possible heart disease, the diagnosis was changed to no heart disease (7) or definite heart disease (5) after review of the CXR and ECG. All 25 patients diagnosed with definite heart disease had this confirmed by abnormal CXR (2), ECG (3), both abnormal CXR and ECG, or echocardiogram (18). CONCLUSIONS: ECG and CXR helped diagnose heart disease in four patients thought to have no heart disease, helped to rule out lesions in seven patients with possible heart disease, helped diagnose heart disease in five patients thought to have possible heart disease, and helped confirm heart disease in nine patients. In these days of cost containment, routine ECG and CXR continue to be valuable tools for the pediatric cardiologist in evaluation of patients with heart murmurs or chest pain. 相似文献
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993.
Modulation of leucine transaminase activity by dietary means 总被引:4,自引:0,他引:4
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995.
Dramatically different phenotypes in mouse models of human Tay-Sachs and Sandhoff diseases 总被引:4,自引:2,他引:4
Phaneuf D; Wakamatsu N; Huang JQ; Borowski A; Peterson AC; Fortunato SR; Ritter G; Igdoura SA; Morales CR; Benoit G; Akerman BR; Leclerc D; Hanai N; Marth JD; Trasler JM; Gravel RA 《Human molecular genetics》1996,5(1):1-14
We have generated mouse models of human Tay-Sachs and Sandhoff diseases by
targeted disruption of the Hexa (alpha subunit) or Hexb (beta subunit)
genes, respectively, encoding lysosomal beta-hexosaminidase A (structure,
alpha) and B (structure, beta beta). Both mutant mice accumulate GM2
ganglioside in brain, much more so in Hexb -/- mice, and the latter also
accumulate glycolipid GA2. Hexa -/- mice suffer no obvious behavioral or
neurological deficit, while Hexb -/- mice develop a fatal neurodegenerative
disease, with spasticity, muscle weakness, rigidity, tremor and ataxia. The
Hexb -/- but not the Hexa -/- mice have massive depletion of spinal cord
axons as an apparent consequence of neuronal storage of GM2. We propose
that Hexa -/- mice escape disease through partial catabolism of accumulated
GM2 via GA2 (asialo- GM2) through the combined action of sialidase and
beta-hexosaminidase B.
相似文献
996.
Background
Overweight and obesity in Australia has risen at an alarming rate over the last 20 years as in other industrialised countries around the world, yet the policy response, locally and globally, has been limited. Using a childhood obesity summit held in Australia in 2002 as a case study, this paper examines how evidence was used in setting the agenda, influencing the Summit debate and shaping the policy responses which emerged. The study used multiple methods of data collection including documentary analysis, key informant interviews, a focus group discussion and media analysis. The resulting data were content analysed to examine the types of evidence used in the Summit and how the state of the evidence base contributed to policy-making.Results
Empirical research evidence concerning the magnitude of the problem was widely reported and largely uncontested in the media and in the Summit debates. In contrast, the evidence base for action was mostly opinion and ideas as empirical data was lacking. Opinions and ideas were generally found to be an acceptable basis for agreeing policy action coupled with thorough evaluation. However, the analysis revealed that the evidence was fiercely contested around food advertising to children and action agreed was therefore limited.Conclusion
The Summit demonstrated that policy action will move forward in the absence of strong research evidence. Where powerful and competing groups contest possible policy options, however, the evidence base required for action needs to be substantial. As with tobacco control, obesity control efforts are likely to face ongoing challenges around the nature of the evidence and interventions proposed to tackle the problem. Overcoming the challenges in controlling obesity will be more likely if researchers and public health advocates enhance their understanding of the policy process, including the role different types of evidence can play in influencing public debate and policy decisions, the interests and tactics of the different stakeholders involved and the part that can be played by time-limited yet high profile events such as Summits.997.
998.
Molecular genetic and phenotypic analysis reveals differences between TSC1 and TSC2 associated familial and sporadic tuberous sclerosis 总被引:14,自引:0,他引:14
Jones AC; Daniells CE; Snell RG; Tachataki M; Idziaszczyk SA; Krawczak M; Sampson JR; Cheadle JP 《Human molecular genetics》1997,6(12):2155-2161
Tuberous sclerosis (TSC) is an autosomal dominant disorder characterised by
the development of hamartomatous growths in many organs. Sixty to seventy
percent of cases are sporadic and appear to represent new mutations. TSC
exhibits locus heterogeneity: the TSC2 gene is located at 16p13.3 whilst
the TSC1 gene, predicted to encode a novel protein termed hamartin, has
recently been cloned from 9q34. With the exception of a contiguous gene
deletion syndrome involving TSC2 and PKD1 , TSC1 and TSC2 phenotypes have
been considered identical. We have now comprehensively defined the TSC1
mutational spectrum in 171 sequentially ascertained, unrelated TSC patients
by single strand conformation polymorphism and heteroduplex analysis of all
21 coding exons, and by assaying a restriction fragment spanning the whole
locus. Mutations were identified in 9/24 familial cases, but in only 13/147
sporadic cases. In contrast, a limited screen revealed TSC2 mutations in
two of the familial cases and in 45 of the sporadic cases. Thus TSC1
mutations were significantly under-represented among sporadic cases
(Fisher's exact p -value = 3.12 x 10(-4)). Both large deletions and
missense mutations were common at the TSC2 locus whereas most TSC1
mutations were small truncating lesions. Mental retardation was
significantly less frequent among carriers of TSC1 than TSC2 mutations
(odds ratio 5.54 for sporadic cases only, 6.78 +/- 1.54 when a single
randomly selected patient per multigeneration family was also included). No
correlation between mental retardation and the type of mutation was found.
We conclude that there is a reduced risk of mental retardation in TSC1 as
opposed to TSC2 disease and that consequent ascertainment bias, at least in
part, explains the relative paucity of TSC1 mutations in sporadic TSC.
相似文献
999.
Knowledge and awareness of risk factors for cardiovascular disease among Canadians 55 to 74 years of age: results from the Canadian Heart Health Surveys, 1986-1992 总被引:2,自引:1,他引:1
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