Heparinized saline or normal saline as a flush solution in intermittent intravenous lines in infants and children

Physical exertions are related to sudden cardiac death following acute myocardial infarction (AMI). Abnormalities in the autonomic modulation during exercise were noted in animals with AMI that were susceptible to potentially lethal arrhythmias. This study was done to evaluate the changes in the autonomic activity during exercise and recovery in AMI patients with good exercise capacity, using spectral analysis of R-R intervals of electrocardiogram (ECG). Symptom-limited treadmill exercise test was done on 17 patients of AMI with mild heart failure (in 7-10 days after the attack) and 21 healthy controls. The exercise was divided into 7 stages; rest, early exercise, mid-exercise, peak exercise, early recovery, mid-recovery, and late recovery. Power spectral analysis of R-R intervals of ECG was performed for each stage. Low frequency (0.04-0.15 Hz) and high frequency (0.15-0.40 Hz) powers, and their ratio were obtained. These parameters were observed throughout the stages in both groups. The trend of their changes during exercise and recovery was essentially the same for both groups; high and low frequency powers progressively decreased during exercise and abruptly increased during early recovery, but did not return to the values at those of rest until 9 minutes into the recovery. When the parameters were compared between the groups, there was a significantly greater decrease of high frequency power during the early exercise (p < 0.05), and a higher ratio of low to high frequency power during the early recovery (p < 0.05) in the patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Direct visualization of individual DNA molecules by fluorescence microscopy: characterization of the factors affecting signal/background and optimization of imaging conditions using YOYO

The cellular mechanisms involved in osteoblast function and bone formation alterations in osteoporosis have been partly elucidated. Recent studies have shown that bone formation abnormalities in various forms of osteopenia result mainly from defective recruitment of osteoblastic cells. These abnormalities in osteoblast function and bone formation are associated with alterations in the expression or production of several growth factors, such as IGFs and TGF-beta, which modulate the proliferation and activity of bone-forming cells. Bone loss related to aging or unloading is characterized by diminished osteoblast proliferation and reduced local concentrations of IGFs and TGF beta. In contrast, estrogen deficiency increases osteoblast proliferation and IGF-I production. These data suggest that alterations in the production of and/or in cell responsiveness to local growth factors may contribute to the bone formation abnormalities seen in these osteopenic disorders. This suggests that preventive or curative treatment with growth factors may be beneficial in osteopenia due predominantly to decreased bone formation. Low doses of IGF-I or TGF-beta have been reported to increase osteoblast recruitment and differentiation, leading to enhanced trabecular bone formation and decreased bone loss in models of osteopenia induced by aging, estrogen deficiency and unloading. A few clinical trials also suggest that low doses of growth factors may stimulate bone formation. Although these findings open up new prospects for the prevention and treatment of osteopenic disorders, progress in this direction awaits the development of factors or analogs that are capable of locally and specifically increasing osteoblast recruitment and differentiation without including side-effects.     

Cranial MR imaging in Wilson's disease

OBJECTIVE: The purpose of the study was to describe the range of abnormalities seen on cranial MR images of patients with Wilson's disease and correlate the findings with clinical severity, duration of disease, and duration of neurologic signs and symptoms before treatment. In those patients with serial studies, the changes on MR images were compared with the clinical response. SUBJECTS AND METHODS: Twenty-five patients with Wilson's disease underwent MR imaging of the brain using conventional spin-echo sequences (n = 25), phase maps (n = 8), and partially refocused interleaved multiple-echo sequences (n = 5). RESULTS: MR imaging findings were abnormal in 22 patients and normal in three patients. The basal ganglia were interpreted as abnormal in 19 (86%) of 22 patients, involving the putamen in 19 (86%), the thalami in 12 (54%), the caudate head in 10 (45%), and the globus pallidus in nine (41%). We found a predilection for involvement of the outer rim of the putamen and the ventral nuclear mass of the thalami. The claustrum was abnormal in three patients. The midbrain was abnormal in 17 (77%) of these 22 patients, affecting predominantly the tegmentum but also the substantia nigra, red nuclei, inferior tectum, and crura. The pons was abnormal in 18 (82%) of 22 patients, and the cerebellum was abnormal in 11 patients (50%), with involvement of the superior and middle cerebellar peduncles. Atrophy was present in 18 (82%) of 22 patients, and cortical white matter changes were apparent in 13 (59%) of 22 patients. The scan of one untreated patient revealed shortening of the T1 relaxation time in the thalami, which was consistent with the paramagnetic effects of copper. Phase maps and partially refocused interleaved multiple-echo sequences performed in eight and five patients, respectively, and used to reveal a susceptibility change induced by iron or copper showed normal findings. We found a significant inverse relationship between severity, but not extent, of change in signal intensity and the length of untreated disease (p = .030) and the total duration of disease (p = .015). The study group was too small to show a correlation with clinical findings. Changes seen on MR images matched the clinical response to treatment in only two of the seven patients who underwent follow-up studies. CONCLUSION: MR imaging revealed abnormalities in the basal ganglia, cerebral white matter, midbrain, pons, and cerebellum. The paramagnetic effects of copper were detected only in untreated patients. Patients with a longer duration of disease had less severe changes in signal intensity. MR imaging was of limited value in follow-up.     

The new toothpastes

Total genomic DNA sampled from 20 oral squamous cell carcinomas (SCCs) and from four SCC cell lines, was examined for genomic imbalances using comparative genomic hybridisation (CGH). Gains and losses of DNA copy number aberrations (CNAs) were found in the primary tumours, but also in the cell lines at a varying number. The patterns of CNAs proved to be rather peculiar in oral SCCs, gains of genetic material clearly dominating compared with losses, and a rather high uniformity of these patterns was an impressive finding. Hypersomies of whole chromosomes, e.g. numbers 17 and 19 or of whole chromosome arms, e.g. 20q, were particularly evident. The segments most frequently gained in oral SCCs were 3q26-q27, 5p15 and 9q34 (16 of 20 tumours each), as well as 1p36.3, 8q24, 10q26, 19 and 20q (15/20 each). Among the 15 tumours with more than 10 CNAs, all showed these imbalances. 11q13 was a band often involved in increases (14/20 tumours), but in several tumours was involved in amplification of DNA copy number. Several other chromosomal segments over represented in more than 60% of the tumours, as, for example, 12q24, 15q22-q24, 16p13.2 and 17q (14/20 tumours each), 6q26-qter, 7p22, 12p12.2-p13, 14q31-q32.2 (13/20) and 1q32-q41, 2q37, 16q23-q24 (12/20 each). In contrast, loss of material affected only a few chromosomal segments, as, for example, 3p12 (12 of the 20 tumours), 5q21 (10/20), 6q13 (8/20). The peculiarities of these findings, in some respect, differ from those found in other epithelial tumours, suggesting a high impact of environmental factors in the generation and progression of these tumours.     

Microtubule organization and stability in the oligodendrocyte

The oligodendrocyte is the glial cell responsible for the formation and maintenance of CNS myelin. Because the development of neuronal morphology is known to depend on the presence of highly organized microtubule arrays, it may be hypothesized that the properties of microtubules influence the form and function of oligodendrocytes. The goals of the present study were to define the physical attributes of microtubules in oligodendrocytes maintained in vitro. The results of electron and confocal microscopy indicate that microtubules are present throughout the cell bodies and large and small processes of oligodendrocytes and are rarely associated with discrete microtubule-organizing centers. A modified "hooking" protocol demonstrated that the polarity orientation of microtubules is uniformly plus-end distal in small oligodendrocyte processes, compared with a nonuniform, predominantly plus-end distal orientation in large processes. Oligodendrocytes were exposed to the microtubule-depolymerizing drug nocodazole to examine microtubule stability in these cells. The results suggest that oligodendrocyte microtubules can be resolved into at least three distinct microtubule populations that differ in their kinetics of depolymerization in the presence of nocodazole. These findings suggest that the properties of the oligodendrocyte microtubule array reflect the functions of the different regions of this highly specialized cell.