Are chest radiographs and electrocardiograms still valuable in evaluating new pediatric patients with heart murmurs or chest pain?

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.     

Comparison of Infasurf (calf lung surfactant extract) to Survanta (Beractant) in the treatment and prevention of respiratory distress syndrome

OBJECTIVE: To compare the relative safety and efficacy of Infasurf (calf lung surfactant extract; ONY, Inc, Amherst, NY, IND #27169) versus Survanta (Beractant, Ross Laboratories, Columbus, OH) in reducing the acute severity of respiratory distress syndrome (RDS) when given at birth and to infants with established RDS. DESIGN: A prospective, randomized, double-blind, multicenter clinical trial. SETTING: Thirteen neonatal intensive care units participated in the treatment arm: seven of these concurrently participated in the prevention arm. PATIENTS: The treatment arm enrolled infants of 相似文献   

The supplementation of culture medium with protease improves the hatching rate of mouse embryos

Mammalian embryos are known to exhibit delayed development and have lower hatching rates in vitro than in vivo because of inadequate culture condition. These discrepancies may be due to a deficiency of the paracrine factors and proteolytic enzymes which exist in the oviduct and uterus. In order to evaluate the effects of proteases on embryonic development and hatching, 2-cell mouse embryos were cultured for 72 h with or without proteases. The addition of 1.0 microg/ml pronase (PE) and/or 0.1 microg/ml proteinase K (PK) did not affect embryonic development up to the blastocyst stage (94.1% versus 88.2%; 92.2% versus 90.2%, respectively) but significantly increased the hatching rate (60.4% versus 39.2%, 71.8% versus 35.3%, respectively). However, the addition of alpha-chymotrypsin (Chymo) was detrimental to embryonic development and hatching. Changes in the structure of the zona pellucida (ZP) structure of embryos which had been cultured in human tubal fluid (HTF) medium with PE and PK were assessed by fluorescein isothiocyanate-conjugated (FITC)-casein. Embryos cultured in HTF-PE and PK were not stained with FITC-casein. When these embryos were cultured within oviducts, their perivitelline space (PVS) became strongly stained with FITC-casein which was easily removed by phosphate- buffered saline washing. This suggests that PE and PK altered the structure of the ZP. We suggest that the addition of PE and PK to culture media may accelerate the hatching of embryo, by structurally altering the ZP and PVS. This may provide a valuable and effective assisted hatching technique for human in-vitro fertilization-embryo transfer.      

Evidence for an X-linked genetic component in familial typical migraine

Migraine is a common complex disorder that shows strong familial aggregation. There is a general increased prevalence of migraine in females compared with males, with recent studies indicating that migraine affects 18% of females compared with 6% of males. This preponderance of females among migraine sufferers coupled with evidence of an increased risk of migraine in first degree relatives of male probands but not in relatives of female probands suggests the possibility of an X-linked dominant gene. We report here the localization of a typical migraine susceptibility locus to the X chromosome. Of three large multigenerational migraine pedigrees two families showed significant excess allele sharing to Xq markers (P = 0.031 and P = 0.012). Overall analysis of data from all three pedigrees gave significant evidence in support of linkage and heterogeneity (HLOD = 3.1). These findings provide conclusive evidence that familial typical migraine is a heterogeneous disorder. We suggest that the localization of a migraine susceptibility locus to the X chromosome could in part explain the increased risk of migraine in relatives of male probands and may be involved in the increased female prevalence of this disorder.      

Electro-encephalogram disturbances in different sleep-wake states following exposure to high environmental heat

In this study, cerebral electrical activity or electro-encephalogram (EEG) was studied following exposure to high environmental heat, in three different age groups of freely moving rats. Each age group was subdivided into three groups: the acute heat stress group, subjected to a single exposure of 4h at 38°C in the biological oxygen demand incubator; the chronic heat stress group, exposed for 21 days, for 1 h each day, at 38°C in the incubator; and the handling control group. The polygraphic sleep-wake recordings involved simultaneous recordings of cortical EEG, electrooculogram (EOG), and electromyogram (EMG), on paper and in digital form on computer hard disk, just after the heat exposure for the acute stressed rats and on the 22nd day for the chronic stressed rats. The power spectrum was calculated for 2s epochs of the EEG signals. Quantitative analyses of EEG (qEEG) showed that, in all three age groups, changes in higher-frequency components (β₂) were significant in all sleep-wake states following both acute and chronic heat stress conditions. The power of β₂ activity in all three age groups after acute heat exposure was significantly decreased during slow wave sleep (SWS) (p<0.05) and rapid eye movement sleep (p<0.05), whereas the reverse was observed in the awake state (p<0.05). Following chronic heat exposure, β₂ activity was found to increase in all three sleep-wake stages in all groups of rats (p<0.01 for SWS in the weaning group and p<0.05 for other data). Thus the study demonstrated that the cortical EEG is sensitive to environmental heat, and alterations in EEG frequencies in different states of mental consciousness due to high heat can be differentiated efficiently by EEG power spectrum analysis.     

Do sequence variants in the major non-coding region of the mitochondrial genome influence mitochondrial mutations associated with disease?

Several different mutations in human mitochondrial DNA (mtDNA) have been associated with disease, but their origins and the basis of the wide phenotypic variability remain to be elucidated. We initially investigated three patients with heteroplasmic disease associated mutations of mtDNA for the presence of cis mutations in the major non- coding region that might influence their origins or pathology. A T --> C transition at nt 16 189 previously identified in one patient with the 3243 G:C mutation was associated with heteroplasmic length variation. Identical length variation was found in patient-derived cybrid lines containing 0-97.5% 3243 G:C. Similarly, heteroplasmic length variation was demonstrated in 2/6 other probands with both the 3243 mutation and the 16,189 polymorphism. The distribution of length variants in probands and in asymptomatic family members was identical in all cases. Thus length variation appears to be independent of the level of 3243 mutant mtDNA and hence probably arose within both 3243 G:C and 3243 A:T mtDNAs. We suggest that the 16,189 polymorphism reflects a predisposition to the formation or fixation of several different mutations in mitochondrial tRNA-LeuUUR.