A simple and effective method of monitoring free muscle transfers: a preliminary report.
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Biomedical subjects
Publications and source records attributed to D Evans.
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The potential value of a bolus injection of ritodrine in the management of fetal distress was examined in 24 patients. Following the injection of ritodrine, uterine activity measured over a period of 14.7 +/- 6.3 (SD) min was reduced to 22 (+/- 12.4 SD)% of the pre-existing values. The cardiotocographic tracings showed a reversion to a normal or less ominous pattern in 14 of the 16 patients where this could be evaluated. The infants in the ritodrine group took less time to establish regular respirations. The perinatal neurobehaviour in the ritodrine and control groups did not differ. Two mothers who were given ritodrine and who received atropine premedication developed tachycardia and marked systolic hypertension. The administration of a bolus of ritodrine may have a place in the management of fetal distress when caesarean section is unavoidably delayed, but atropine premedication must be avoided as the combination can lead to potentially serious cardiovascular complications.
Labelling of cellular RNA by [32P]orthophosphate can be enhanced up to a factor of three by adding 2 to 10 X 10(-5)M of non-labelled nucleosides to the culture medium. The lag period of labelling can be reduced by a factor of two. Adenosine has the highest effect, while uridine is without effect. Labelling of viral RNA, which occurs in the cytoplasm, is reduced by nucleosides, suggesting that two precursor pools of nucleoside triphosphates are differently affected. The base composition of the labelled RNA cannot be influenced by incubation with non-labelled nucleosides. As a possible explanation for this observation a group translocation transport mechanism is discussed.
The intracellular sites of biosynthesis of the structural proteins of murine hepatitis virus A59 have been analyzed using cell fractionation techniques. The nucleocapsid protein N is synthesized on free polysomes, whereas the envelope glycoproteins E1 and E2 are translated on the rough endoplasmic reticulum (RER). Glycoprotein E2 present in the RER contains N-glycosidically linked oligosaccharides of the mannose-rich type, supporting the concept that glycosylation of this protein is initiated at the co-translational level. In contrast, O-glycosylation of E1 occurs after transfer of the protein to smooth intracellular membranes. Monensin does not interfere with virus budding from the membranes of the endoplasmic reticulum, but it inhibits virus release and fusion of infected cells. The oligosaccharide side chains of E2 obtained under these conditions are resistant to endoglycosidase H and lack fucose suggesting that transport of this glycoprotein is inhibited between the trans Golgi cisternae and the cell surface. Glycoprotein E1 synthesized in the presence of monensin is completely carbohydrate-free. This observation suggests that the intracellular transport of this glycoprotein is also blocked by monensin.
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This paper reports preliminary findings in a convenience sample of one half the population enrolled in a study of self-management in low income families where a child has asthma. In initial evaluation data, parents participating in self-management education reported significantly less fear and anxiety associated with their children's wheezing episodes than did control families. They also reported that their children exhibited fewer signs of stress during wheezing episode. A trend toward reduced school absences and emergency room visits was noted among participating families. The actions taken by a family to manage the illness increased with the number of sessions attended.
Information on several variables, including occupational history and various coronary risk factors, was collected from the wives of 568 married men who died of coronary heart-disease (CHD) and an equal number of matched control subjects. The crude matched-pair relative risk of fatal CHD among men who retired compared with non-retirees was 2.9 (95% confidence limits from 1.9 to 4.9). After adjustment for age and history of hospitalisation for myocardial infarction by means of a paired multiple-logistic regression analysis the relative risk was reduced to 1.8 (range 1.0 to 3.3). These data suggest that retirement and subsequent coronary mortality may be linked.
One newborn child was selected from 14 families in which kwashiorkor had occurred. Undernutrition in this test group was prevented for the first two years of life by the provision of supplementary feeding. Controls who were the siblings directly preceding each of the 14 test children received no supplementary feeding, but received medical attention and management. In each family an older child who previously had kwashiorkor (kwashiorkor group), and the nearest sibling who had received neither extra feeding nor medical management (kwasiorkor control group) were also available for comparison. A battery of psychologic tests was administered when the mean age of the test group was 8.9 years. The mean full-scale IQ of the supplementary feeding group at an average age of 8.9 years was significantly higher than that of any of the other three groups. There was no significant difference between test and control groups on nonverbal IQ. Measures of "brain damage" did not discriminate between any of the four groups. The results suggest that nutritional factors contribute especially to the elevation of verbal intelligence. Environmental stimulation (daily contact with a more alert child) apparently contributed to the elevation of the nonverbal scores of the controls.
Three hundred seventy-two (63%) of 590 enrollees in nine smoking cessation workshops held over a five-year period responded to a follow-up survey. Outcome data were collected retrospectively for six-month intervals from workshop to follow-up. Forty nine per cent of all enrollees graduated, and 56% of the respondents quit smoking during the program. Nonsmoking rates declined to an average of 25% by the first year post-workshop and remained relatively stable thereafter for periods up to five years.
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Patient education provides a vehicle for increasing the self-management of chronic illness and promoting modifications of life styles, which are considered important strategies for prevention. Evaluating the impact of such programs is complex and poses a number of methodologic and technical problems. Outcome measures of patient education programs are defined and reviewed in terms of the existing evaluation literature and our own studies utilizing diabetes as a prototype condition. Important dimensions of adaptation are outlined and indices to measure it discussed in an effort to examine aspects of educational programs directed at facilitating coping and maintaining quality of life. Factors which influence outcome variables are identified and include: patient factors (e.g., age, ethnic, socioeconomic, cultural, personality, and emotional), disease factors (e.g., severity of illness, age of onset, length of illness, mode of therapy), system factors (e.g., patient's location in the health care system, relation of teaching program to other health care providers). The effects of these factors are described including their implications for research design.
In vesicular stomatitis virus New Jersey serotype polyacrylamide gel electrophoresis was unable to distinguish the polypeptides of the temperature-sensitive (ts) mutants of complementation groups A, B, C, and F from those of the wild-type virus. However, the NS polypeptide of the representative mutant of group E, ts E1, had a significantly greater electrophoretic mobility than that of the wild-type virus NS polypeptide. The electrophoretic mobilities of the NS polypeptides of the three mutants of complementation group E varied, being greatest in the case of ts E1, slightly less for ts E2, and only a little greater than that of wild-type virus NS polypeptide in the case of ts E3. Since the NS polypeptides of the revertant clones ts E1/R1 and ts E3/R1 have mobilities identical to that of wild-type NS polypeptide, the observed altered mobilities of the group E mutants are almost certainly the direct result of the ts mutations in the E locus. The electrophoretic mobilities of the intracellular NS polypeptides of the group E mutants were indistinguishable from those of their virion NS polypeptides. The electrophoretic mobilities of the NS polypeptides of the group E mutants synthesized in vitro using mRNA synthesized in vitro by TNP were identical to those of the NS polypeptides of their purified virions. The NS polypeptides of all three mutants were labeled with (32)P(i) to approximately the same extent as wild-type virus NS polypeptide, indicating that gross differences in phosphorylation of this polypeptide are unlikely to account for the altered mobilities. We propose a model in which the NS polypeptide consists of at least three loops held in this configuration by hydrophobic or ionic forces or both and stabilized by phosphodiester bridges. If a mutation affects one of the amino acids to which the phosphate is covalently linked, the phosphodiester bridge cannot be formed, and, as a result, in the presence of sodium dodecyl sulfate the affected loop opens and thus the NS polypeptide migrates further into the gel. Such a configuration may also explain the multifunctional nature of the NS polypeptide.
A high proportion of peritoneal cells from untreated mice, after 4--5 days in culture, develop into plaque-forming cells against bromelain-treated mouse red blood cells. The number of plaque-forming cells was increased significantly by exposing the peritoneal cells to ammonium chloride to lyse red blood cells before culture. Conversely, the increase was significantly inhibited by adding before culture untreated or bromelain-treated sheep or mouse red blood cells. Treated or untreated horse or rat red blood cells did not inhibit the increase. Treating peritoneal cells or subpopulations of peritoneal cells with anti-theta serum and complement before culture caused a significant increase in the number of plaque-forming cells against bromelain-treated red blood cells after 3--4 days of culture. Various procedures were used to fractionate peritoneal cells into B-cell enriched and B-cell depleted subpopulations before culture and after culture, to investigate whether some of the plaque-forming cells could be attributed to phagocytic cells. Generally, changes in the number of plaque-forming cells against bromelain-treated mouse red blood cells paralleled changes in B-cells. In some experiments the proportion of plaque-forming cells observed represented up to 85% of the B-cells present. The results suggest that the high level of autoreactivity is due to antibody production by B-cells and that phagocytic cells are not forming spurious plaques. Further, it appears that the autoimmunity is regulated by T-cells and can also be inhibited by mouse RBC.
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