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Biomedical subjects

D L Armstrong

Publications and source records attributed to D L Armstrong.

At least 127 records · Page 7Linked to original sources
PubMed1980

Morphology of the developing visual cortex of the human infant: a quantitative and qualitative Golgi study.

A renaissance of the Golgi impregnation method has focused interest on dendritic aspects of neuronal development. The visual cortices of 39 "neurologically normal" infants from 14 weeks' gestation to 6 months of age were prepared at postmortem for rapid Golgi impregnation studies. These were stained and duplicated with camera lucida drawings. The total number of cells in defined columns of the visual cortex was counted on cresyl violet-stained sections, and differentiated neurons were identified. The number of spines on the apical and basal dendrites of selected cells was counted for a given interval along the dendrites. The camera lucida drawings, cell counts, and spine counts were used to illustrate the normal ontogeny of the visual cortex.

Cell Count↗
PubMed1979

An electron microscopic study of childhood dermatomyositis.

Muscle biopsies from 12 patients with a typical clinical picture of dermatomyositis have been examined by electron microscopy. Endothelial cells of intramuscular blood vessels, their basal lamina, pericytes, muscle fibers, and satellite cells show degenerative or regenerative alterations. In nine patients, tubular arrays were noted in the cisterns of endoplasmic reticulum of endothelial cells, pericytes, lymphocytes, macrophages and satellite cells. Other types of inclusions were also observed. The pathogenesis of the disease is discussed.

Adolescent↗
PubMed1979

The kinetics of tubocurarine action and restricted diffusion within the synaptic cleft.

1. The kinetics of tubocurarine inhibition were studied at the post-synaptic membrane of frog skeletal muscle fibres. Acetylcholine (ACh) and (+)-tubocurarine were ionophoresed from twin-barrel micropipettes, and the membrane potential of the muscle fibre was recorded intracellularly. Tubocurarine-receptor binding was measured by decreases in the response to identical pulses of ACh. 2. The responses to both ACh and tubocurarine had brief latencies and reached their maxima rapidly. It is suggested that under these conditions the kinetics of tubocurarine action are not slowed by diffusion in the space outside the synaptic cleft. 3. After a pulse of tubocurarine, recovery from inhibition proceeds along a roughly exponential time course with a rate constant, 1/tau off approximately equal to 0.5 sec-1. This rate constant does not depend on the maximal level of inhibition and varies only slightly with temperature (Q10 = 1.25). 4. After a sudden maintained increase in tubocurarine release, the ACh responses decrease and eventually reach a new steady-state level. Inhibition develops exponentially with time and the apparent rate constant, 1/tau on, is greater than 1/tau off. When the steady-state inhibition reduces the ACh response to 1/n of its original level, the data are summarized by the relation, 1/tau on = n(1/tau off). 5. When the ACh sensitivity is reduced with cobra toxin, both 1/tau on and 1/tau off increase. Thus, the kinetics of tubocurarine inhibition depend on the density of ACh receptors in the synaptic cleft. 6. After treatment with collagenase, part of the nerve terminal is displaced and the post-synaptic membrane is exposed directly to the external solution. Under these circumstances, 1/tau off increases more than tenfold. 7. Bath-applied tubocurarine competitively inhibits the responses to brief ionophoretic ACh pulses with an apparent equilibrium dissociation constant, K = 0.5 microM. 8. In denervated frog muscle fibres, extrasynaptic receptors have a lower apparent affinity for tubocurarine. After a pulse of tubocurarine, inhibition decays tenfold more rapidly at these extrasynaptic sites than at the synapse. 9. It is suggested that each tubocurarine molecule binds repeatedly to several ACh receptors before escaping from the synaptic from the synaptic cleft and that the probability of this repetitive binding is enhanced because the nerve terminal presents a physical barrier to diffusion out of the cleft. Consequently, the receptor transiently buffer the concentration of tubocurarine in the cleft, and the macroscopic kinetics of inhibition are much slower than the molecular binding rates for tubocurarine.

Acetylcholine↗
PubMed1978

Subcortical leukomalacia. Relationship to development of the cerebral sulcus and its vascular supply.

The development of the microvascular architecture of the cerebral cortex and white matter was studied in the preterm, term, and older infant, using postmortem cerebral angiography and metal impregnation studies. During the first few months after birth, a relatively avascular triangle forms in the white matter at the depth of the sulcus. Subcortical leukomalacia occurs in this triangle as well as in border zones between the major cerebral arteries.

Brain↗
PubMed1978

Brain biopsies for neurodegenerative disease in children.

Brain biopsies for neurodegenerative disease performed at The Hospital for Sick Children, Toronto, over a 12-year period (1964 to 1976) were reviewed. Of 64 biopsies, major histologic abnormalities with diagnostic or prognostic significance comprised 39% of the total cases, minor abnormalities represented 13%, and 48% appeared normal. The procedure failed to provide prognostic assistance in 41%. With the advent for newer diagnostic techniques (enzyme assays and muscle, skin, peripheral nerve, rectal, and appendix biopsies) for neurodegenerative disease in childhood, a much lower yield is noted (15 to 20%). Only two progressive degenerative childhood conditions remain in which cerebral tissue is necessary for diagnosis--Alexander disease and Canavan spongy degeneration.

Adolescent↗
PubMed1978

Peripheral median nerve damage secondary to brachial arterial blood gas sampling.

Examination at 18 months post-term of 139 infants of birth weight less than or equal to 1,500 gm revealed 18 instances (13%) of persistent median nerve damage. All affected infants had received frequent percutaneous brachial artery punctures as neonates. Block sections of the cubital fossa done at autopsy on 12 randomly selected very low-birth-weight infants showed perineural hemorrhage, and Wallerian degeneration or traumatic neuroma of the median nerve in eight patients. It is recommended that brachial artery punctures be avoided whenever possible in the neonatal period.

Autopsy↗
PubMed1977

Management of craniopharyngioma in children.

The authors review 48 cases of craniopharyngioma in children treated during 25 years, 1950 to 1975. Complete excision of the tumor, attempted in 23 patients, was possible in 17. The authors advocate aggressive treatment aimed at complete excision of the tumor, using radiotherapy only when adherence of the tumor to the internal carotid artery precludes total excision, and symptoms recur.

Adolescent↗
PubMed1976

Central nervous system patholgoy associated with mask ventilation in the very low birthweight infant: a new etiology for intracerebellar hemorrhages.

Mask-applied ventilatory support was noted to cause severe head molding in infants with birthweights under 1,501 gm. To determine if this molding was detrimental to the infant, the neonatal course and autopsy findings were reviewed for 106 infants. Twenty significant intracerebellar hemorrhages were found. An association between these hemorrhages and mask-applied positive pressure ventilation was demonstrated (P = .05). This relationship was maintained when all cases of generalized bleeding dyscrasia were removed (P = .021). It is proposed that the distortional forces produced by the mask attachment, together with the buffeting effect of intermittent positive-pressure ventilation, are causally related to the production of intracerebellar hemorrhages by direct contusion, by ischemic stasis, or by altered venous drainage. The authors urge strong caution when dealing with the small premature infant in using any attachment device that causes molding of the cranial vault, particularly in the occipital area.

Birth Weight↗
PubMedDate not supplied

Ethanol and diazepam inhibition of hippocampal LTP is mediated by angiotensin II and AT1 receptors.

Angiotensin II (AII) inhibits the induction of hippocampal long-term potentiation (LTP), a frequency-dependent model of learning and memory. These results demonstrate that the dose-dependent inhibition of LTP due to ethanol (EtOH) and diazepam (DZ) involves AII. Inhibition of LTP induction by AII, EtOH, and DZ can be blocked by AII receptor antagonists saralasin and lorsartan (DuP 753). Lorsartan is a competitive antagonist of the AT1 subtype AII receptor. Therefore, the EtOH and DZ inhibition of LTP induction is mediated by AT1 receptors. These results indicate a new role for AII in the brain in the possible mediation of memory deficits associated with alcohol and the benzodiazepines.

Animals↗
PubMedDate not supplied

Role of the paraventricular nucleus in the projection from the nucleus of the solitary tract to the olfactory bulb.

Electrophysiological experiments were performed on anesthetized rats to determine the effects of lesions of the paraventricular nucleus on the amplitude of evoked potentials recorded in the periglomerular layer of the olfactory bulb after nucleus of the solitary tract electrical stimulation. Lesions of the paraventricular nucleus enhance the amplitude of both the positive and negative components of the evoked potential in the olfactory bulb. The pathway from the paraventricular nucleus to the olfactory bulb seems to exert a suppressive influence over the projection from the nucleus of the solitary tract to the olfactory bulb under these conditions.

Animals↗
PubMedDate not supplied

Responses of lateral hypothalamic neurons recorded in vitro to moderate changes in glucose concentration.

Single unit neuronal activity of lateral hypothalamic neurons was recorded extracellularly in hypothalamic slices. Glucose concentration in the perfusate was modified in small amounts to simulate normal physiological glycemic fluctuations associated with feeding. Several neurons responded reliably under these conditions. These data on simulated small glycemic changes, based on observations in the whole animal, suggest that the modulation of neuronal activity reported in this study is a result of a direct action of glucose on cells in this region of the hypothalamus.

Animals↗
PubMedDate not supplied

Double pituitary glands with partial duplication of facial and fore brain structures with hydrocephalus.

A female term infant was born with multiple bony and facial abnormalities involving the mandible, palate, tongue, nasopharynx, vertebrae, ribs and brain. Death occurred at 1 week and a rare combination of forebrain anomalies, were found in a big head, with complete agenesis of the corpus callosum with duplication of the infundibulum, pituitary, anterior third ventricle and aqueduct. The CAT scan was diagnostic of agenesis of corpus callosum. Incomplete twinning or incompetent neural induction with genetic and epigenetic factors have been suggested as possible mechanisms responsible for this rare malformation.

Abnormalities, Multiple↗
PubMedDate not supplied

Losartan reduces ethanol intoxication in the rat.

Results of a previous study showed that ethanol inhibition of hippocampal long-term potentiation (LTP) induction was mediated by angiotensin II (AII) and the AT1 subtype receptor because it was blocked by losartan, a specific AT1 antagonist. Because LTP is an important hippocampal function involved in the memory process and other behaviors, it is possible that losartan might block some of the directly observable ethanol-induced changes in rat behavior. Results demonstrate that losartan can effectively block some of the intoxicating effects of low doses of ethanol, 2 g/kg PO or IP. However, even a high dose of losartan 20 mg/kg IP, did not reduce significantly any of the intoxicating effects of the higher dose of 4 g/kg administered by gavage. Higher doses of ethanol might be more difficult to block because of a direct effect on the post synaptic membrane.

Alcoholic Intoxication↗
PubMedDate not supplied

Angiotensin II antagonists block ethanol effects on the aerial righting reflex.

The purpose of the present study was to determine the effects of an angiotensin II (AII) AT1 antagonist, losartan 10, 15, and 20 mg/kg IP, and the AII AT2 antagonist, PD 123319, 20 mg/kg IP on ethanol (EtOH) intoxication as measured by the aerial righting reflex in male rats. EtOH (25%), 2.0 g/kg, was administered by stomach tube under mild metaphane anesthesia and the aerial righting reflex was determined at 30-min intervals for 3.5 h. The AII antagonists were administered IP 2 h before the EtOH. There were six groups of 10 rats each: EtOH alone, 10, 15, or 20 mg/kg losartan plus ethanol, 20 mg/kg losartan plus 20 mg/kg PD 123319 plus EtOH, and 20 mg/kg losartan alone. Data were analyzed by a two-way ANOVA with repeated measures on one factor, time. Results show a clear intoxicating effect of ethanol on the aerial righting reflex that was blocked significantly by losartan in a dose-dependent way. Losartan alone had no observable effect. The administration of both antagonists, losartan and PD 123319 injected IP in two different sites, completely blocked the EtOH effect on the aerial righting reflex. The involvement of AII in the mediation of EtOH intoxication effects on the aerial righting reflex supports results of our previous studies on the effects of EtOH on open field behavior, AII impairment of the retention of an inhibitory shock avoidance response, and AII inhibition of hippocampal granule cell long-term potentiation, all of which can be blocked by losartan.

Angiotensin II↗
PubMedDate not supplied

Life-threatening congestive heart failure as the presentation of centronuclear myopathy.

Myocardiopathy is associated infrequently with centronuclear myopathy. We present biopsy studies of a 15 1/2-year-old black male who presented with profound acute congestive heart failure and diffuse muscular atrophy. Cardiac symptoms had been present for 6 months; limb weakness had been unassociated with either infantile hypotonia or developmental delay. Cardiac catheterization demonstrated a dilated myocardiopathy and poor left ventricular contractility. Biopsies of both ventricles revealed striking hydropic degeneration and fibrosis. Right triceps biopsy disclosed centronuclear myopathy. Because the spectrum of disease expression in centronuclear myopathy is extensive, an association with cardiac disease always should be considered in these patients. In addition, we recommend that patients who present with idiopathic myocardiopathy should be evaluated for this and other skeletal muscle diseases.

Adolescent↗
PubMedDate not supplied

Rett syndrome: cerebellar pathology.

The cerebellar pathology at autopsy of 5 patients with Rett syndrome is described. The patients ranged in age from 7-30 years. All had markedly reduced brain weights with proportionately small cerebella. Microscopic examination revealed loss of Purkinje cells, atrophy, astrocytic gliosis of the molecular and granular cell layers, and gliosis and loss of myelin in the white matter. Cortical atrophy occurred focally along the folia and was often more marked in the tips of the folia. The 2 oldest patients had been treated with phenytoin which may have contributed to the morphologic changes. Atrophy and gliosis increased with age or in patients without phenytoin treatment; the youngest patient demonstrated only minor microscopic changes. In addition to the generalized alterations, 1 patient had several adjacent folia with severe atrophy. The results indicate that cerebellar changes in Rett syndrome consist of general hypoplasia with the addition of atrophy beginning in childhood and progressing over many years.

Adolescent↗
PubMedDate not supplied

Brain calcification in hypoxic-ischemic lesions: an autopsy review.

Calcification of ischemic lesions in a child's brain is well recognized by pathologists; however, clinicians and radiologists usually associate cerebral calcification with infections, particularly the TORCH organisms. We illustrate this phenomenon in a 5-month-old infant with extensive, calcified, multicystic encephalomalacia without evidence of a cerebral infection. In order to ascertain the incidence of cerebral calcification in pure hypoxic-ischemic lesions, we retrospectively analyzed 486 consecutive autopsies. Ninety-nine patients had histologic evidence of cerebral hypoxic-ischemic lesions and hypoxia or ischemia. Thirty-nine of these patients displayed microscopic calcification; 23 patients had slight, 12 had minor, and 4 had prominent calcifications. Prominent calcification lesions were large enough to be detected by routine radiologic methods. Correlations between degree of calcification and the underlying disease process and between the gestational age and the length of survival were not statistically significant. This study illustrates the very frequent occurrence of brain calcification in ischemic brain lesions in children. It is necessary to include this diagnosis in the differential diagnosis of cerebral calcification.

Adolescent↗