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Biomedical subjects

W J Logan

Publications and source records attributed to W J Logan.

At least 37 records · Page 2Linked to original sources

Continuous and intermittent measurement of intracranial pressure by Ladd monitor.

Controversy exists as to whether the force of application of the sensor of the Ladd monitor to the anterior fontanelle affects the accuracy of measurements of intracranial pressure. To resolve this problem, an artificial fontanelle was constructed and fontanelle pressure measurements were recorded at varying forces of application of the sensor. This in vitro technique demonstrated that anterior fontanelle pressure measured with the Ladd monitor is dependent on the force of application. Measurements of anterior fontanelle pressure were made in 17 infants and were correlated with simultaneous direct intracranial pressure measurements. These in vivo measurements confirmed the findings on the artificial fontanelle. Both the in vivo and in vitro measurements suggest that an application force of 7 to 10 gm on the sensor will produce an accurate reflection of intracranial pressure. We describe two devices with which the sensor may be applied to the fontanelle with constant measurable force: one for intermittent measurement and another for continuous recording.

Cranial Sutures↗

Multimodal electrophysiological assessment of ataxia telangiectasia.

We report multimodal evoked response studies in eleven children with ataxia telangiectasia. The ABRs were normal in all but one patient despite the severity of the disorder. The SERs were abnormal in all of the patients, the waveforms being either absent or of delayed latency, the abnormalities were more marked in the older patients. Abnormal motor and sensory nerve conduction studies were also found in all but the younger few patients. Most notably, the VERs were abnormal in all but 2, the older patients had delayed VERs and most had small amplitude responses. The electrophysiological profile of ataxia telangiectasia patients on the multimodal evoked responses differs from that found in certain other degenerative ataxias studied and may have some diagnostic utility.

Adolescent↗

Hexose transport in L6 muscle cells. Kinetic properties and the number of [3H]cytochalasin B binding sites.

(1) Myoblasts in culture (L6 cell line) were used as an in vitro model system, to study the kinetic and pharmacological properties of hexose transport in skeletal muscle tissue. (2) Uptake of 2-deoxy-D-[3H]glucose into L6 cells grown in monolayer culture was judged rate limiting since: (2) The time course of sugar uptake extrapolated to zero, (b) a parallel inhibition of hexose uptake and phosphorylation was caused by cytochalasin B, and (c) very little backflow of the hexose was detected. (3) Uptake of 2-deoxy-D-[3H]glucose by cells in monolayers was linear for at least 20 min and it was stimulated by countertransport. The Kt value was 0.83 mM. Cytochalasin B inhibited uptake non-competitively, and half maximal inhibition was achieved at 0.3 microM. Cytochalasin E (up to 5 microM) did not affect 2-deoxy-D-[3H]glucose uptake. (4) L6 myoblasts, detached by trypsinization, retained the hexose transport activity. Kt in detached cells was 0.96 mM. V was 3.2 nmol/min per mg protein, and half maximal inhibition was observed with 0.25 microM cytochalasin B. (5) [3H]Cytochalasin B binding to detached cells showed saturable and non-saturable components. The former could be further separated into cytochalasin E-sensitive binding (probably associated to cytoskeletal proteins) and cytochalasin E-insensitive binding, a fraction of which was inhibited by D-glucose. The D-glucose sensitive sites amount to 16.3 pmol/mg protein, and showed a Kd of 0.49 microM, which is in close agreement with the Ki of cytochalasin B inhibition of hexose uptake. These sites probably are equivalent to the hexose carrier molecules, and are present at a density of 6.8 . 10(6) sites/cell.

3-O-Methylglucose↗

Regulation of amino acid transport in L6 myoblasts. II. Different chemical properties of transport after amino acid deprivation.

The mechanism of stimulation of amino acid transport system A caused by amino acid deprivation in L6 cells was investigated. In cells loaded with alpha-aminoisobutyric acid (AIB), amino acid deprivation increased the rate of proline uptake only after the intracellular [AIB] dropped below 7 mM. Efflux of proline was not sensitive to the presence of proline in the outer medium (with or without external Na+), suggesting that efflux through system A (and possibly uptake) is not susceptible to transinhibition. Transport (stimulated uptake) into amino acid-deprived cells and that into amino acid-supplemented cells differed in several chemical properties: 1) In the former group, transport was higher at lower pH values than in the latter, and the optimum pH values were 7.5 and 7.8, respectively. 2) Unlike proline uptake in supplemented cells, uptake in deprived cells was inhibited by 50% with N-ethylmaleimide (1 mM) or by 50 microM p-chloromercuribenzoate (PCMBS). Inhibition by PCMBS was not due to collapse of the Na+ gradient. The mercurial inhibited only the deprivation-induced stimulation of transport, bringing the rate of proline uptake to the "basal" uptake level observed in amino acid-supplemented cells. Proline uptake was not stimulated by a second deprivation following treatment with PCMBS and a supplementation-deprivation cycle. However, in untreated cells, or by reversing mercaptide formation with dithiotreitol, the second deprivation stimulated transport. Deprivation at 4 degrees C did not elicit stimulation of proline uptake. Cycloheximide prevented the stimulation and decreased the rate of proline uptake in deprived cells more efficiently than in supplemented cells. Actinomycin D prevented stimulation when added at the onset of deprivation. The above data indicate that stimulation of transport by deprivation is protein synthesis-dependent and that the stimulated transport had chemical properties distinct from the "basal" transport in supplemented cells. The evidence presented is consistent with a model of activation of a finite pool of transporters upon deprivation, the chemical characteristics of which differ from those of the "basal" transport system.

4-Chloromercuribenzenesulfonate↗

Specific uptake of norepinephrine and dopamine by homogenates of rat cerebral cortex after locus ceruleus lesion.

Unilateral injection of 6-hydroxydopamine into the locus ceruleus led to long lasting depletion of norepinephrine in the ipsilateral parietal cerebral cortex of the rat up to 8 weeks after injection. The uptake of both norepinephrine and dopamine by homogenates of parietal cortex was decreased markedly on the ipsilateral, but not on the contralateral, side. The uptake of four other neurotransmitter candidates or precursors was unaffected by the lesion. Desipramine (DMI) markedly inhibited the uptake of both norepinephrine and dopamine by cortical preparations from the contralateral side and from control rats, but this effect was not seen in preparations from the norepinephrine-depleted, ipsilateral cortex. The decreases DMI-sensitive uptake of norepinephrine or dopamine was highly correlated with decreased norepinephrine in the ipsilateral cortex. These results suggest that the specific uptake of norepinephrine and dopamine is a valid marker of noradrenergic innervation of the parietal cortex and that dopamine seems to be accumulated primarily by norepinephrine terminals in this region. Two and 8 weeks after locus ceruleus lesion, a DMI-insensitive, benztropine-sensitive dopamine uptake becomes apparent in ipsilateral cortical preparations, This may represent proliferation or increased function of dopaminergic cortical projections, compensating for noradrenergic denervation.

Animals↗

A syndrome of infantile CNS degeneration.

We describe six patients from five families, who have a syndrome that, to our knowledge, has not been previously reported. The syndrome is characterized by growth failure, ophthalmoplegia, optic atrophy, choreoathetosis, areflexia, hypotonia, dysmorphic facies, and severe mental and motor retardation. Some of the children also had microcephaly and seizures. The clinical course is remarkably uniform and slowly progressive. The abnormalities first noted are delayed psychomotor development and poor weight gain, and the others all develop within the first three years of life. The syndrome seems to be hereditary. Extensive laboratory investigation has not yielded an etiology. Until pathologic material is available, the disorder remains a syndrome and the diagnosis is established by the unique combination of neurological abnormalities.

Adolescent↗

Erythrosin B inhibition of neurotransmitter accumulation by rat brain homogenate.

A mixture of seven food dyes inhibited the accumulation of eight neurotransmitters or neurotransmitter precursors by rat brain homogenate. At a low concentration (1 microgram per milliliter), erythrosin B (FD&C red 3) was the only dye that inhibited dopamine accumulation. Erythrosin also was effective in decreasing the accumulation of all the other transmitter substances, suggesting that the inhibition is nonspecific and probably secondary to general membrane alteration.

Animals↗

Central nervous system maturation in the stressed premature.

The developmental sequence of sleep cycles has been found to be a useful index of central nervous system maturation in premature infants. To determine the effects of severe reversible stress on the maturation of sleep cycles, 6- to 8-hour sleep studies were done on 10 premature infants with severe hyaline membrane disease (HMD) and 10 healthy premature babies. The studies were done in the neonatal intensive care unit and included patients from 30 weeks' gestation to term and in all stages of the disease. Prior studies were confirmed showing that percentage of quiet sleep increases, transitional sleep changes little, and active sleep decreases from 30 weeks' gestation to term. In infants with severe HMD, the percentage of quiet sleep was less and active sleep higher than in unstressed infants of similar age who acted as controls. Once the infants recovered from HMD, sleep patterns became similar to those found in the control group. These data suggest that when respiratory distress occurs in the premature infant, there is a transient delay in central nervous system maturation as measured by sleep cycle analysis.

Brain↗

Two spontaneous BALB/c lymphomas synthesize IgM: monomers and half molecules are isolated and characterized whereas another molecule resembles IgD.

Spontaneous lymphomas of BALB/c mice, both in vivo tumors and cell lines established in long term tissue cultures, were investigated for their ability to synthesize IgM by using radiolabeled amino acid precursors. Immunoglobulins manufactured by lymphomas K46 and L10A had the m.w. of monomeric IgM and IgM half molecule. Both of these molecules could be immunoprecipitated with class-specific anti-IgM but not anti-IgA or anti-IgG. When precipitated with polyvalent anti-Ig L10A synthesized monomeric immunoglobulins that migrated as two peaks in contrast to their single counterpart precipitated with anti-IgM. The second peak migrated in the region expected for IgD. Monomer and half molecules were composed of similar ratios of mu-chains to light chains linked by disulfide bonds. The mu2L2 monomer of these B cell lines migrated slightly slower in SDS PAGE than a mu2L2 secreted by a myeloma. Thus, these lymphomas synthesize immunoglobulins with the chemical and antigenic characteristics typical of monomeric membrane-attached IgM and IgM half molecules, plus a molecule resembling IgD on L10A only. Lymphoma assembly of monomeric IgM may follow the same initial biosynthetic sequence as myeloma assembly.

Animals↗

Clear-cell sarcoma of tendons and aponeuroses.

The natural history and histologic characteristics of a rare malignant neoplasm of tendons and aponeuroses are described, and a case is presented which originated in the right foot of a 19-year-old Caucasian woman who succumbed to the disease after 4 years. This case represents the first known example of metastasis to the oral cavity of this particular neoplasm.

Adult↗

Amino acid neurotransmitter candidates: sodium-dependent high-affinity uptake by unique synaptosomal fractions.

Glutamic and aspartic acids and glycine are accumulated by high-affinity uptake systems into synaptosomal preparations in central nervous tissue. Sodium is required by these high-affinity transports, but not by the low-affinity transports for these and other amino acids. The sodium-requiring amino acid uptake systems label unique synaptosomal fractions. Observations suggest that these amino acids serve specific synaptic functions, presumably as neurotransmitters.

Amino Acids↗