Central metatarsal shortening following osteotomy and its clinical significance.
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Biomedical subjects
Publications and source records attributed to J Morgan.
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We have confirmed that the loss of muscle strength in 12 boys with Duchenne's muscular dystrophy, as measured by manual muscle testing, approximates a linear decay model, but we have also found that it fits as well a first order decay model. The strength in the same eight muscles was measured over time. Results of an analysis of 111 examinations are reported here. An arbitrary numerical scale for grading muscle strength was used, such that normal was 13 units, and no movement was zero. The maximal sum, if all 8 muscles were normal, would be 104 units. Pooling all measurements, the linear decay rate in this sum was -0.189 +/- 0.023 (estimate +/- standard error) arbitrary muscle strength units . month-1. The corresponding first order fractional decay rate was -0.0034 +/- 0.0004 month-1. However, a more detailed statistical analysis indicated that decay rates in muscle strength were not homogeneous, i.e. muscle strength decayed faster in some patients than others. The decay constants in 11 of the 12 subjects spanned a 10-fold range, and in one subject increased the spread to 40-fold. The distribution frequency of decay rates appears to be bimodal. In these assessments, the muscle strength at time zero was not known. Therefore, an estimate of muscle strength at 10 years was made. This varied from 34 to 71 units. The group mean was 53.0 units using the exponential model, i.e. on average, only 51% (= 53.0/104 X 100) of the normal muscle strength remained in the 8 muscle groups assessed at age 10 years. In conclusion, a quantitative characterization of muscle strength deterioration is reported, which emphasizes the heterogeneity in this disease. This approach may eventually allow quantitative distinctions between Duchenne's and Becker's varieties of muscular dystrophy.
A series of tris-maleate-buffered salt solutions, from pH 6.4 to 8.9 was used to assess the effect of pH on the two hour leakage of creatine kinase (CK) from isolated mouse heart. Leakage was directly related to pH. Hourly enzyme leakage was minimal (less than 0.25%) at pH 6.4, but from pH 6.4 to 8.9, it increased more than 10 fold. The pattern of fractional leakage in the second hour, relative to pH, was approximately sigmoidal in shape, and similar to a monoprotic titration curve. This observation suggests that a single proton binding site may govern myocardial enzyme leakage, under the conditions of this study. Similar observations were made using salt solutions, buffered with tris-HCl, from pH 7.3 to 8.6. The functional group of this putative protective site has a pKa of approximately 7.9, and properties consistent with a nitrogen base of the type found in terminal amino, epsilon-amino, and/or imidazolium groups.
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Aluminium hydroxide is used to prevent hyperphosphataemia in patients undergoing dialysis, but many standard preparations are unpalatable. In this study hydrated aluminium sucrose was suspended in synthetic cream and used as a biscuit filling. Six patients undergoing dialysis took part in five five-week study periods comparing different forms of treatment. No significant difference was found between serum phosphate concentrations measured during standard treatment and those measured during treatment with aluminium sucrose biscuits. There was no significant difference in serum phosphate concentrations when the patients were given placebo biscuits and when they received no treatment. Aluminium sucrose presented in this form was an adequate phosphate binder and was acceptable to the patients.
The effects of active nonspecific immunotherapy were studied in 42 patients receiving daily iv Corynebacterium parvum at 2 mg/m2 in 14-day courses and in 14 patients receiving iv methanol extraction residue of BCG (MER) at 0.5 mg/m2 weekly. The host defense evaluations included measurement of the number of adherent macrophage precursors per milliliter of blood (monocyte adherence), serum lysozyme, and antibody-dependent cell-mediated cytotoxicity (ADCC) of peripheral blood mononuclear cells to chicken red blood cells (CRBC) or human red blood cells (HRBC). During a single course of C. parvum, monocyte adherence did not rise significantly, whereas ADCC of peripheral blood mononuclear cells to CRBC and HRBC rose significantly (15.7-49.9% and 34.8-53.5% lysis of target cells, respectively). However, after a mean of 4.5 months on therapy, monocyte adherence increased an average of 7.5-fold. During weekly MER therapy, monocyte adherence, serum lysozyme, and ADCC of peripheral blood mononuclear cells to CRBC rose significantly within 4-7 days after the first dose (3.8-8.7 adherent cells/ml blood x 10(4), 7.6-10.8 microgram, and 34.4-41.4% target cell lysis, respectively). The host defense parameter, which was subnormal in the cancer patients (monocyte adherence), was boosted into the normal range in all the deficient patients by iv MER. The host defense parameters, which were normal or slightly elevated in the patients before therapy (serum lysozyme and ADCC of peripheral blood mononuclear cells to CRBC and HRBC), were hyperactivated above the upper limit of the normal range in 71.4, 71.4, and 50% of the patients, respectively, by iv MER. These methods can quantitatively reflect activation of monocytes and killer cells by C. parvum and MER and may be useful for evaluation and quantitation of both active nonspecific and immunorestorative immunotherapy in general.
In the study energy expenditure measurements have been made by open circuit calorimetry on a number of occasions on four infants, with special reference to the energy cost of resting metabolism, activity and diet-induced thermogenesis. In addition, for two subjects the energy cost of growth was determined. The energy expended with respect to activity was highly variable among all subjects and it was postulated that this was a factor of great importance in the energy balance of young infants; indeed, the effect of diet-induced thermogenesis was enhanced by activity. A calculation of the total energy required to gain 1 g of wet tissue in two infants was found to be different. As their intakes were 'low' and 'high' though their weight gains were accelerated and slow respectively, the difference in the energy cost of growth has been discussed as a reason for this paradox.
Recent studies of job satisfaction, working conditions, and changes in the content of work indicate that problems of low productivity and dissatisfaction may be related to changes in the organization of work which have reduced the amount of autonomy and control which workers have over the labor process. At the same time, elements in the labor movement, which has traditionally focused almost exclusively on obtaining higher wages and greater benefits for union members, now seem to be directing their attention to issues of workplace democracy and worker control over the production process and company policies. The research reported here investigates the determinants of worker autonomy and of workers' desire for increased worker control over the workplace. This article describes what are viewed as the main hypotheses suggested by earlier research and reports the findings and new hypotheses derived from a preliminary analysis of data from the ISR National 1977 Quality of Employment Survey and pilot in-depth interviews with sixteen Baltimore workers.
The plasma levels of creatine kinase (CK), lactate dehydrogenase and alkaline phosphatase were determined in normal mice of the white CF1 and black C57Bl/6 strains, and in clinically normal, heterozygous and dystrophic mice of the C57BL/6J-dy strain. CF1 mice, 13-130 days old, had an average plasma CK of 152 +/- 58 mIU/ml (mean +/- standard deviation) (n=19). Mice of the C57BL/6 strain had a CK of 164 +/- 39 mIU/ml (n=5). Dystrophic mice, younger than 80 days, had an average CK of 1186 +/- 609 mIU/ml (n=16). The CK levels in plasma from 3 dystrophic mice (99, 99 and 156 days) were 182, 267 and 169 (mean 206) mIU/ml, respectively. CK activities in known heterozygotes (+/dy), 180-200 days old, were 165 +/- 156 mIU/ml (n=7). Up to 80 days of age, 14 clinically normal littermates of dystrophic mice showed two distinct groupings of CK activity. Four animals had a mean of 1136 +/- 418 mIU/ml, while 10 others had a mean CK of 173 +/- 116 mIU/ml. The reasons for the 4 elevated values have yet to be established. Over 80 days of age, the average CK was 152 +/- 63 mIU/ml (n=5). When compared statistically, only the young (less than 80 days) dystrophic and four clinically normal animals, with elevated CK levels, were significantly different from the other six groups of mice examined (p less than 0.001). The data indicate that the plasma CK level in C57BL/6J-dy dystrophic mice is elevated, at least up to about 11 weeks.
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We outline methods for identifying DNAs containing sequences complementary to specific mRNAs, and provide a number of complementary approaches for mapping the arrangement of mRNAs along the DNA. These methods, together with S1 nuclease mapping and the direct visualization of R-loops with the electron microscope, provide a comprehensive approach to defining the architecture of mRNAs coding for specific polypeptides and the arrangement of RNA transcripts along the genome. This detailed cartographic information can then be used to study the steps in the processing of mature mRNAs and determine the modes by which the expression of specific genes is regulated.
In this review the question of obesity in the pre-school child has been examined in three areas of interest: first, the extent of our knowledge of food intake and its relationship to growth in the young child; secondly, the difficulties in defining obesity on a practical level in this group, and thirdly the constraints in the examination of energy balance because of the limitations of techniques available for this type of work. The conclusion is that studies are needed to analyse factors regulating energy balance, and thereby explain why, in the very young child, there is an individual difference in the utilization of energy for growth, activity and basal processes.
To obtain an accurate record of an individual's food intake in the assessment of his nutritional status is a difficult task. To obtain such a record for an infant is more difficult still, involving the close cooperation between the investigator and the infant's mother. Why there has been little progression in methodology from the earliest days of recording individual food intakes is discussed and areas of improvements are suggested. Accuracy could be improved if techniques were streamlined and objectives more clearly defined. Dietary surveys could provide data of value to other workers in the field by using conventions in data collection and in the reporting of results.
The efflux of the enzymes, creatine kinase (CK) and lactate dehydrogenase (LDH) from isolated normal and dystrophic mouse (C57BL/6J-dy) skeletal muscle and heart has been studied. Older (5-9 months) dystrophic mouse triceps contained only 63% of normal CK. At 3.5-10 weeks, dystrophic gastrocnemii had 72% and 61% of normal for males and females, respectively. By 5-7 months, the levels dropped to only 26% and 15% of normal. When skeletal muscle efflux was normalized to enzyme content, dystrophic muscle was not significantly different from normal for the first three hours, and was lower than normal in the 3-5 hour period. This was true for both triceps and gastrocnemius. Similarly, no difference in LDH efflux from gastrocnemius was seen between control and dystrophic mice. In contrast, there was no difference in enzyme concentration of normal and dystrophic hearts. Despite this, hearts from dystrophic mice had a higher efflux of both CK and LDH in the first three hours, but not beyond. The results indicate that under the conditions of these studies, dystrophic skeletal muscle was not, but heart was, more permeable to muscle enzymes than normal muscle.
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One hundred consecutive patients undergoing aorta-coronary bypass grafting (ACBG) alone, without ventricular venting, were prospectively studied to determine the incidence and consequence of perioperative myocardial infarction (PMI) and the clinical variables that were predictive of PMI. Incidence was determined by serial electrocardiography (ECG) 100 patients; serum CK, GOT, and LDH (100 patients). CK isoenzymes (qualitative 100 patients, quantitated 50 patients); vectorcardiography (VCG) (78 patients); and 99mtechnetium pyrophosphate scintigraphy (TcPyp) (52 patients). The incidence of PMI by ECG was 9%; an additional 8% of cases was diagnosed by enzymes alone. The incidence of diagnostic change by VCG was 19% and by scintigraphy, 25%. Using at least one changed variable of the remaining three as the reference standard, the relative sensitivity and relative specificity of given variables in the diagnosis of PMI were as follows: ECG 67% and 100%, respectively; VCG 85% and 94%; scintigraphy 92% and 97%; and serum enzymes 86% and 96%. By univariate analysis, unstable angina was the only significant predictor of PMI. The operative mortality rate was 2% and the mortality rate at 12 months was 5%. There was a significantly greater mortality rate in patients with PMI diagnosed by ECG (p less than 0.01), in patients with unstable angina pectoris before operation (p less than 0.05), and in women (p less than 0.05).