Creativity in developmentally disabled adolescents.
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Biomedical subjects
Publications and source records attributed to J Rowe.
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The enzyme anthranilate-5-phosphoribosylpyrophosphate phosphoribosyltransferase from Serratia marcescens was purified to apparent homogeneity. The purification procedure included ammonium sulfate precipitation, DEAE-cellulose chromatography, Sephadex gel filtration and hydroxyapatite chromatography. The molecular weight of the native protein as determined on a calibrated Sephadex G-200 column was 45000. Dodecylsulfate-polyacrylamide gel electrophoresis in the presence of reducing agent revealed a subunit molecular weight of 43000 +/- 900, suggesting that the enzyme exists as a monomer. The sequence of the amino-terminal 38 residues revealed that three amino amino acids, glutamine (six residues), glutamic acid (five residues) and serine (five residues) comprised 42% of the sequence composition.
Aqueous extracts of mouse submaxillary glands yield six peaks on Sephadex G-75 columns, each containing several molecular species. Two of these fractions (III and IV) have a profound effect on the immune response. When given a day before immunization with sheep erythrocytes, the number of antibody-producing cells is reduced ten-fold or more, and the switch from IgM to IgG is virtually absent. Administration two days before or on the day of immunization results in about 50% depression; outside this range there is no effect. The dose-response curve is of sigmoid shape, with the median at about 0.5 mg of fraction III/40 g mouse, reaching an asymptote after doses of greater than or equal to 5 mg at about 5% of the response of untreated mice. Depression of the primary response does not prevent the development of immunological memory: the secondary response is typical in the early and predominant appearance of IgG-producing cells, although their numbers are somewhat lower than in the controls which received no treatment before primary immunization. Treatment on the day before boosting abrogates the secondary response. The immunotranquilizer from mouse submaxillary glands acts equally well on syngeneic and allogeneic recipients, affecting the earliest stage of the immune response. The results are compatible with the induction of a temporary block in the development of helper T cells.
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Milieu therapists are confronted with a dilemma when more than one child in the same family requires hospitalization. Conventional wisdom discourages simultaneous hospitalization of siblings on the same unit. The sibling bond, however, is an important aspect of development and can be used therapeutically. This paper examines issues and opportunities presented to milieu therapists by the simultaneous hospitalization of siblings, and makes recommendations for maximizing therapeutic use of the sibling bond.
The responses of siblings to a childhood mental illness have been conceptualized in different ways. When siblings have not been ignored, they have been viewed most frequently as an influence upon the illness or as subject to the same dynamics that were believed to have caused the mental illness. As conceptualizations of the causes of mental illness have changed, the literature on siblings has changed to focus on the impact of the illness on the sibling. How siblings and sibling relationships are conceptualized has important implications for clinical research and practice. More research is needed to understand the sibling experience in childhood mental illness. Clinicians can do more for the family if all of the family dynamics and responses to the illness are explored.
A patient is described who developed symptomatic sinus bradycardia as low as 20 beats per minute and sinus arrest of up to 4.4 seconds while receiving guanethidine, 75 mg daily. The bradycardia resolved following discontinuation of the drug and reappeared upon challenge with it. Intrinsic disease of the sinoatrial and atrioventricular nodes was evidenced 3 weeks following discontinuation of the guanethidine by a borderline abnormally prolonged sinus node recovery time of 1500 msec and a PR interval of 0.28 seconds. Although sinus bradycardia is a known and not infrequent side effect of guanethidine, such an extreme form as seen in our patient appears to be quite rare, and may be related to the pre-existing disease of the conduction system.