Transient erythroblastopenia.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Gordon.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Intellectual and other neuropsychological dysfunctions have been observed in survivors of childhood acute lymphocytic leukaemia (ALL). The possible relationship of therapy to these dysfunctions was investigated in a prospective study of children with newly diagnosed ALL seen at the Children's Hospital of Philadelphia. They were evaluated with standardised intelligence tests during the first month of treatment and periodically thereafter. There were two therapy schedules--one using standard drugs for induction and maintenance, the other a more intensive schedule. Central-nervous-system prophylaxis (2400 rad cranial radiation and six doses of intrathecal methotrexate) was given to all. Significant reductions were found in overall IQ score for the majority of children, younger patients being most affected. More extensive testing of surviving children, with and without decline in IQ, all of whom were normal on the first test, revealed patterns of functional deficits and residual strengths that could not be characterised with IQ testing alone. These deficits, which could affect learning and academic performance, were not seen in six children studied years after receiving similar chemotherapy that included intrathecal and oral methotrexate but not cranial irradiation.
The administration of morphine to rats at room temperature is reported to suppress serum thyrotropin (TSH) levels by a hypothalamic mechanism. However, it is unknown whether endogenous opioid peptides (EOP) are involved in the control of TSH secretion. The present studies show that naloxone (10 mg/kg, i.p.) an opiate-receptor antagonist, prevented the decline in rat serum TSH which occurs with heat exposure. Morphine sulfate (20 mg/kg, i.p.) treatment prevented the cold-induced elevation in serum TSH and pretreatment with haloperidol (0.3 mg/kg, i.p.) eliminated morphine's influence. Medial-basal hypothalamic thyrotropin-releasing hormone (TRH) content, measured by RIA, increased in the morphine-treated rats which were exposed to 4 degrees C. A submaximal intravenous dose of TRH (300 ng/100 g) was given to determine whether morphine suppresses serum TSH through the release of hypothalamic thyrotropic inhibitors. Morphine pretreatment did not alter TSH stimulation by TRH. Morphine alone or combined with TRH did not alter basal or stimulated TSH secretion in vitro. These studies strongly suggest that, in rats, the EOP modulate TSH secretion under conditions such as acute heat exposure which was associated with a decline in serum TSH. Under specific circumstances, the suppression of serum TSH by morphine may be dopamine-dependent.
Mice were injected from day of birth onward with rabbit anti-mouse IgM antiserum or purified rabbit anti-mouse IgM antibodies. These mice completely lacked Ig-positive cells or serum Ig, as analyzed by specific fluoresceinated antibodies on the fluorescence-activated cell sorter (FACS-II), by polyclonal B cell mitogens and by specific precipitation in agar. These animals were then primed in vivo by antigen emulsified in complete Freund's adjuvant, and, subsequently, their draining lymph nodes were tested for their T cell proliferative responses in vitro, to the relevant antigen and were found to be severely impaired. However, the antigen-presenting capacity of both spleen cells and thioglycollate-induced peritoneal cells was found to be intact.
Explore the source record for details and available documents.
A basic question about visual perception is whether the retina produces a faithful or a distorted neural representation of the visual image. It is now well known that in some retinal pathways there are significant nonlinear transductions which distort the neural image. The next natural question is, What are the locations of the nonlinear stages within the retinal network? We report here on an investigation of linearity and nonlinearity of responses of horizontal cells in the turtle retina as an assay of the degree of nonlinearity in the outer plexiform layer of the retina. The visual stimuli were sinusoidal gratings; these patterns were modulated by contrast reversal with a sinusoidal time course. The conclusion from our experiments is that the turtle's horizontal cell responses show evidence only of linear spatial summation even at moderately high contrasts on moderately high background levels. Our work thus indicates that there is no significant distortion of the visual image by the photoreceptors or by the neural summation of photoreceptor signals by horizontal cells under normal physiological conditions. These results are consistent with the view that the major nonlinearities of the retina are proximal to the outer plexiform layer.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Lymph node cells obtained from a case of non-Hodgkin's lymphoma, of follicular center cell histology, were seen by immunofluorescence to express immunoglobulin mu heavy chains but no detectable light chain on their surfaces. Antibody specific for determinants expressed only on uncombined mu-chain reacted with these cell surfaces, but not with normal or neoplastic cells expressing surface IgM. Analysis of radioiodinated surface material revealed mu-chains which, without reduction, migrated on SDS-gel electrophoresis as normal mu-chain monomers, and again failed to detect light chains. Lysates of cells incubated with 3H-leucine revealed the synthesis of mu-chains but not of light chains. The labeled mu-chains were not secreted into the culture supernatant, a finding confirmed in parallel cultures by radioimmunoassay. The findings are discussed with particular reference to current concepts of the "mu-chain only" phenotype.
Explore the source record for details and available documents.
Experiments were carried out on guinea-pig L2C leukaemic lymphocytes to investigate the mechanism of antigenic modulation of their surface immunoglobulin (Ig) defined as the conferring by anti-Ig of resistance to lysis by anti-Ig plus complement. The phenomenon reflects, and is probably a consequence of, redistribution of the Ig molecules by bivalent antibody. Fab fragments of the antibody were completely ineffective. Parallel studies by indirect immunofluorescence of the movement of th surface antigen-antibody complexes revealed that modulation for syngeneic complement was apparent when the complexes were minimally aggregated: capping and extensive endocytosis were not necessary. Modulation for xenogeneic (rabbit) complement required more extensive movement but was still appreciable while complexes persisted on the surface. Sodium azide at 10 mM, which inhibits antibody-induced redistribution of surface molecules, diminished modulation. In experiments omitting pre-incubation with antibody alone, the presence of azide during incubations with anti-Ig plus syngeneic complement increased lysis from a low and variable to a consistently high level; there was no effect on the already high level of lysis occurring with the non-modulating anti-Ia plus syngeneic complement. This effect of azide provides further evidence that antigenic modulation can be a major factor determining a cell's survival when it is confronted simultaneously by antibody and complement.
Following previous authors, the term antigenic modulation is used to describe the induction, by antibody, of resistance to lysis by antibody plus complement. A report is given of the rapid antigenic modulation in vitro of surface immunoglobulin (Ig) on guinea-pig L2C leukaemic lymphocytes: incubation of the cells for 2 min or longer at 37 degrees with anti-Ig diminished or removed completely the lysis occurring during subsequent incubation with anti-Ig plus complement. The modulation was effective for both xenogeneic (rabbit) and syngeneic (guinea-pig strain 2) complements, but more rapid for the latter. It appeared simply to require the action of antibody on a metabolically active cell: no requirement could be demonstrated for any serum component other than antibody, and there was a need to raise the temperature to 37 degrees after attachment of the antibody. There was molecular specificity inasmuch as modulation with anti-Ig failed to confer any resistance to lysis by another antibody (anti-Ia) plus complement.
Explore the source record for details and available documents.
Structural differences between normal and pale, soft, exudative (PSE) longissimus dorsi (LD) muscle from purebred and crossbred pigs were observed using scanning and transmission electron microscopy. The effect of severe freeze-thaw contraction on the muscle samples was observed. The membranes of many different organelles (sarcoplasmic reticulum, mitochondria, sarcolemma and connective tissue) appeared markedly disrupted after cryofracture of PSE muscle with frequent breaks especially near the Z-lines. In addition, there was little definition of the M-line and H-zones in either the PSE or intermediate animals.
We measured the visual sensitivity of the conger eel retina by means of its electroretinogram (e.r.g.) and whole nerve responses. The spectral sensitivity of the retina closely corresponded to a prediction based on the density spectrum of the conger visual pigment, measured in situ. The pigment density in the conger eel retina is high, perhaps as high as 1.0. Thus, the predicted spectral sensitivity would be much broader than is observed if the absorption spectrum of the pigment governed the visual sensitivity. The reason why the visual spectral sensitivity corresponds to the density spectrum and not to the absorption spectrum is that the photoreceptors in the conger eye are arranged in tiers and only the inner tier contributes to vision.
Explore the source record for details and available documents.