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B H Landing

Publications and source records attributed to B H Landing.

At least 19 recordsLinked to original sources
PubMed1998

Developmental patterns in the cytoarchitecture of the human cerebral cortex from birth to 6 years examined by correspondence analysis.

This paper uses correspondence analysis to examine the developmental patterns in the cytoarchitecture of the human cerebral cortex from birth to 72 months. The study is based on data collected by the late J. L. Conel, which consist of over 4 million individual measurements of six microscopic neuroanatomic features for each of six cortical layers in 46 cytoarchitecturally distinct regions. We analyze 1,727 profiles of development over eight age-points (term birth, 1, 3, 6, 15, 24, 48, and 72 postnatal months) resulting from the combinations of neuroanatomic feature, cortical layer, and brain cytoarchitectural region in the Conel data. The profiles for any given combination of feature and layer are found to be remarkably similar in all regions of the brain, and therefore the developmental patterns of different cytoarchitectural regions are not distinguishable from one another. Developmental change is most rapid at the earlier stages; of the total change in profile patterns observed, more than one-third occurs between birth and 6 months, about one-third occurs between 6 and 15 months, and less than one-third occurs between 15 and 72 months. The majority of the variance in developmental profiles is accounted for by the six microscopic, neuroanatomic features. Correspondence analysis shows that Conel's data are highly consistent and reliable.

Aging↗
PubMed1998

Evidence for a postnatal doubling of neuron number in the developing human cerebral cortex between 15 months and 6 years.

The generalization of the finding of no postnatal neurogenesis in non-human primates to humans may be incorrect because: (1) rhesus macaques belong to a superfamily that diverged more than 25 million years ago from the superfamily including the genus Homo; (2) the pulse thymidine labeling method, which demonstrates DNA synthesis rather than mitosis per se, is less reliable than some have assumed. This study examines changes in the number of neurons in a column underneath a cortical surface area of 1 mm2, extending through all cortical layers (mm2-column) for 35 gyri (representing about 73% of the human cerebral cortex) based on the data of J.L. Conel (1939 to 1967). We corrected these data, derived from his measures of cortical neuronal packing density, somal breadth and height, and cortical layer thickness at postnatal ages 0, 1, 3, 6, 15, 24, 48, and 72 months, for shrinkage and stereological errors. In all 35 gyri, neuron number/mm2-column: (1) initially declines (mu = 46% decline, sigma = 8%), 95% of which is due to surface area expansion (mean age of nadir value = 15.8 months); (2) then increases to age 72 months by 70% (mu = 1.7-fold increase, (mu rate = 1.1% per month). Because of a a concomitant 1.3-fold increase in cortical surface from 15 to 72 months, total cortical neuron number increases 2.2-fold. The close agreement between neuron number/mm2-column for Conel's age 72-month data to the corresponding values reported by others for adult human and primate cortex using more modern methods suggests the finding is not an artifact. Neuronal proliferative fate-determining factors provide at least four mechanisms for increasing cortical neuron number postnatally, with or without DNA synthesis.

Aging↗
PubMed1998

Quantitative microscopic anatomy, illustrated by its potential role in furthering understanding of the processes of structuring the developing human cerebral cortex.

In this study, we searched for patterns in selected, quantitative microscopic features of the developing postnatal human cortex for 35 cytoarchitectural areas at eight age points from birth to 72 months. These data come from the largest extant survey of the microscopic features of the developing postnatal human cerebral cortex (JL Conel, 1939-67). In contrast to Jacobson's proposal that cortical surface area increases in proportion to brain weight, Conel's data show that surface area increases as brain weight2/3, with the maximal rate of increase in both brain weight and cortical surface area occurring from 1 to 3 months. We computed the numbers of cortical neurons per cortical layer under 1 mm2 of cortical surface (neurons/layer per mm2 column) and divided these values by the total neuron number/mm2 column. For all areas, these data show plateaux in most of the layers for periods of months to years, often preceded and followed by changes in their neuron number in a sinusoidal fashion. The age points of the maxima and minima of such laminar values differ across the 35 cortical areas, indicating that their sinusoids are phase-shifted with respect to each other. Ranking the six layers in each area at each age point by their neuron number/layer per mm2 column shows that, by 72 months, the first areas to receive thalamic auditory or visual input (primary sensory and unimodal association cortices) have the most neurons in layer 4 and in either layer 3 or 6. In contrast, by 72 months, other areas have the most neurons in layers 3 and 6, with the primary motor cortex reaching this ranking earlier than any other area. For temporal and parietal association areas, layers 2 (short cortico-cortical connections) and 4 (thalamo-cortical connections) have the most neurons from birth to 6 months, whereas layers 3 (long cortico-cortical connections) and 6 (cortico-thalamic connections) have the most neurons by 72 months. The quantitative, statistically non-random patterns demonstrated by our analyses suggest that hierarchical correlations between such structural changes and age-specific behavioral acquisitions exist during the first 72 months of postnatal development.

Cerebral Cortex↗
PubMed1998

Constructing the human cerebral cortex during infancy and childhood: types and numbers of cortical columns and numbers of neurons in such columns at different age-points.

This study examines JL Conel's data on neuron numbers in 35 human cortical areas for eight age points from 0 (birth) to 72 months, to analyze cortical columns, the presumed functional units of the cortex. For each cortical area at each age point, cortical surface divided by the square root of the area's neuron number gives cross-sectional areas with radii ranging from 180 microns at birth to 250 microns at 72 months. For the prefrontal cortex at birth and 48 months, these radii are approximately 2.10 and 1.19 times the longest radial basal dendrites, suggesting similar dimensions between these two measures of column radius. The logarithm of neuron number per cortical area and age point was examined in relation to the Weber-Fechner law governing the relationship between stimulus intensity and perception. A mechanism for this law consistent with the cortical model of Douglas et al. illustrates the importance of local circuit neurons. The cross-sectional areas of hexagonal columns for prefrontal cortex, using as radius, the longest radial extent of layer 5 pyramidal neuron basal dendrites, ranging from 0.013 mm2 at birth to 0.064 mm2 at 48 months, suggests that functional cortical columns increase cross-sectional area during development. These cross-sectional areas are 55-100-fold larger at birth, and 229-277-fold larger at 48 months, than those computed from somal width in prefrontal, layer 5 pyramidal neurons. Comparison of radial extent of pyramidal basal dendrites to their soma-to-soma distances shows that layer 3 pyramidal basal dendrites reach 1.5 and 4.0 other pyramidal neurons at 15 and 60 months, respectively, while layer 5, extra-large pyramidal basal dendrites reach 1.14 and 1.72 other such neurons at birth and 48 months, respectively. If such a relationship holds for other cortical areas, then the Conel data can be used to estimate basal dendrite extent, for which there currently is a paucity of data.

Aging↗
PubMed1998

Increased submucosal nerve trunk caliber in aganglionosis: a "positive" and objective finding in suction biopsies and segmental resections in Hirschsprung's disease.

OBJECTIVE: To establish the diagnostic usefulness of submucosal hypertrophic nerve trunk morphology in Hirschsprung's disease as a quantifiable parameter supportive of aganglionosis on hematoxylin-eosin-stained sections. DESIGN: We retrospectively evaluated size and density of submucosal nerves on hematoxylin-eosin-stained sections and S100 protein-stained sections of resected segments from 13 patients with Hirschsprung's disease, and in sections of 20 aganglionic and 50 ganglionic rectal suction biopsies. SETTING: All patients were seen at Childrens Hospital Los Angeles (Calif), a tertiary-care pediatric center; the age of patients at diagnosis or resection ranged between 2 days and 3 years. RESULTS: Aganglionic segments contain many distinct nerve trunks greater than 40 microm in diameter. Ganglionic segments/biopsies showed no nerve trunk larger than this threshold value (P approximately .0000). Nerve trunks of such caliber are rarely encountered in pathologic transition zones and sites of colostomy. CONCLUSIONS: Submucosal nerve trunks that are 40 microm or greater in diameter strongly correlate with abnormal innervation/aganglionosis. Use of this objective parameter in evaluating suction biopsies should be helpful in the morphologic diagnosis of Hirschsprung's disease in infancy and early childhood.

Biopsy, Needle↗
PubMed1995

Tay-Sachs disease with atypical chronic course and limited brain storage: alpha-locus hexosaminidase genetic compound.

A 19-year-old Irish-Jewish male had a slow neurologic regression starting at age 4 1/2 years with stuttering. The chronic course resembled that of Spielmeyer-Vogt (juvenile ceroid-lipofuscinosis) disease. The brain was atrophic with neuronal losses and huge compound inclusions in the remaining neurons. Lipid NANA was within normal limits in gray and white matter and GM2 gangliosides were moderately elevated at 11.5% lipid NANA. Beta-hexosaminidase A activity was reduced, secondary to a compound mutation at the alpha-locus. Lysosomal hydrolase activities and lipid composition showed nonspecific abnormalities. Exhaustive tissue extraction ruled out the possibility of tightly bound gangliosides to account for the relatively low GM2 ganglioside concentration. The extract contained unidentified chromogenic substances interfering with the resorcinol reaction. The similarly affected patient's sister lived to age 26 years and her brain was even more atrophic. No biochemical abnormality to account for progressive neuronal losses and relative lack of GM2 ganglioside storage was found.

Adult↗
PubMed1994

Cardiomyopathy in childhood and adult life, with emphasis on hypertrophic cardiomyopathy.

Over 60 entries in the genetic catalog have cardiomyopathy features--32 autosomal dominant, 35 autosomal recessive and X-linked. Over 40 present in, or can have survival into, adult life. Major clinicopathologic categories of these cardiomyopathic disorders included: sudden death (13 entities); cardiac conduction disturbance important feature; associated myopathy or motor dysfunction; storage diseases with cardiac involvement; cardiac amyloidoses; and, other categories. Genes, abnormality of which can cause hypertrophic cardiomyopathy (HCM), have been identified on chromosomes 1, 14 and 15, the locus on chromosome 14 involving the B-myosin heavy chain gene, but at least one unidentified locus is known to exist and there is a suggestive locus on chromosome 16, so that HCM is not a single disease but a group of disorders with clinicopatholopic similarities. To investigate these aspects of HCM in some detail, sixty-six patients with "sharply demarcated" differential myocardial fiber bundle hypertrophy (DMBH), considered to be of significant degree, from a pediatric autopsy data base of approximately 8,000 cases, were reviewed. Twenty-three of the patients died suddenly, without antecedent significant cardiac dysfunction, seven had clinical congestive heart failure of varying duration, three were stillborn, six showed evidence of aspiration of amniotic sac content (three had history of fetal distress), five had ischemic bowel disease, three (two with clinical cerebral palsy and one with Ondine's curse syndrome) had cerebral atrophy and sclerosis and one had extensive more acute encephalomalacia, and a variety of other major "causes of death" were present. Whether all infants and children with DMBH meeting the criteria used, who do not have congenital heart disease, have dominant hypertrophic cardiomyopathy (HCM) cannot be established by studies of this type, but the "concentration" of a gene or genes for HCM in pediatric autopsy series because the strong effect of HCM on life expectancy is relevant to this possibility. The data raise the question that stillbirth, fetal distress with aspiration of amniotic sac content, ischemic bowel disease and cerebral atrophy and sclerosis may be hitherto underappreciated features of HCM in childhood, and that patients with HCM may be peculiarly liable to die with certain types of septic shock, such as acute meningococcemia. In the material of this study, sudden death was statistically more frequent in females than in males in childhood (p < .029).

Adolescent↗
PubMed1993

Studies of the enteric nervous system in Alzheimer disease and other dementias of the elderly: enteric neurons in Alzheimer disease.

Studies of the myenteric (Auerbach) plexus of esophagus, stomach, small intestine, colon, and rectum, by microdissection and pointcount morphometry, for 18 patients with Alzheimer disease (AD), eight with other types of dementia of the elderly, non-demented elderly patients, and younger control patients, show a normal loss of enteric neurons and plexus mass with age, comparable to that reported by others for rats and guinea pigs. Values for patients with AD or other non-AD dementias did not differ from those for elderly controls. Enteric neurons in AD or the other dementias studied showed no definite stain with ALZ-50, a monoclonal antibody to a derivative of the microtubule-associated protein tau, which stains degenerating cerebral neurons in AD. Although the processes in the central nervous system in AD affect some neurons derived from the neural plate, the results of this study suggest that the enteric neurons, which are of neural crest origin, are not affected in AD. Enteric neurons, at least by the methods of this study, do not provide a useful peripheral marker for AD.

Age Factors↗
PubMed1992

Lupus nephritis: prognostic factors in children.

As newer treatment modalities become available for patients with severe lupus nephritis, it becomes increasingly important to identify patients at risk for renal failure. In this study, the records of 90 children presenting with systemic lupus erythematosus over a 13-year period were reviewed. Nineteen were lost to follow-up prior to completion of the study. Of the 71 remaining children, 16 (22%) progressed to chronic renal failure. Persistent hypertension lasting greater than 4 months, anemia, abnormalities of the urinalysis, and elevated serum creatinine level were significantly associated with progression to renal failure. Sex, race, age, abnormalities of creatinine clearance, and 24-hour urine protein collection were not associated with progression to renal failure. Renal biopsies were obtained in 45 children. Biopsies were initially classified according to World Health Organization criteria. Diffuse proliferative glomerulonephritis was significantly associated with progression to renal failure. The 45 biopsies available were reviewed by one of the authors and categorized by activity and chronicity indices. Both the active lesions of fibrinoid necrosis, synechiae, tubular casts, and vasculitic lesions and the chronic lesion of glomerular sclerosis correlated with progression to renal failure. Of the 16 children who progressed to renal failure, 2 had cadaver kidney transplants and are well 5 years posttransplant; 4 had fulminant lupus and died within 1 month of commencing dialysis; 10 began chronic dialysis. Five of the 10 children on chronic dialysis died from sepsis. These data suggest that children with systemic lupus erythematosus who undergo dialysis do poorly.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗
PubMed1991

The question of parallax-effect on radiographic assessment of short trachea in infants and children.

Disproportionately short trachea, can be recognized in AP chest radiographs of infants and older children taken during quiet respiration and showing an evaluable air tracheobronchogram, by the thoracic vertebral level of the carina (normally at T4 in neonates and infants, and at T5 in children two years of age or older). To establish the extent to which a parallax-effect of differing angles of X-ray beam relative to the patient can influence the radiologic assessment of carinal level, we measured the tracheal-vertebral distance at the carina in 29 lateral radiographs of neonates, infants and children, prepared diagrams of the loci of carinal beam intercept of the vertebral column for different angles of beam to body, from tracings of lateral radiographs of two 2-week-old infants, one with trachea of normal length and one with short trachea; of a nine-year-old child with short trachea, and of a ten-year-old with normal trachea, and made radiographs of a postmortem tracheobronchogram of a two-day-old infant at different beam angles. We conclude that tube-body angles of the order of 10-15 degrees from vertical at 27 inches (68.6 cm) or at 40 inches (101.6 cm) FFD do not significantly affect the apparent thoracic vertebral level of the carina in AP chest radiographs, and that a beam angle of 20 degrees or more from vertical is necessary to change the apparent level of tracheal bifurcation by one vertebral body, depending on the patient's age and on whether the patient's position relative to the X-ray beam is lordotic or anti-lordotic.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1990

Diagnostic aspects and syndromal associations of short trachea with bronchial intubation.

Conditions with disproportionately short trachea, with a reduced number of tracheal cartilage rings and a high level of tracheal bifurcation, have been reported. We have seen accidental bronchial intubation in nine patients with short trachea. This risk can be reduced by recognition of conditions associated with short trachea, by awareness that methods for calculating endotracheal tube length from body length can overpredict tube length for patients with short trachea, and when feasible, by use of preintubation chest roentgenograms showing air bronchograms to establish the thoracic level of tracheal bifurcation. Twelve patients with short trachea, four with bronchial intubation, and six conditions not previously associated with short trachea, are reported. Three of the patients also had laryngeal hypoplasia.

Child↗
PubMed1990

Serial section-reconstruction of anomalous tracheobronchial branching patterns from CT scan images: bridging bronchus associated with sling left pulmonary artery.

The use of the technique of wax-plate serial section-reconstruction, based on contiguous axial plane CT images of the upper thorax, to prepare a replica of the central air-way (trachea and major bronchi) of an infant with sling left pulmonary artery type 2B, with bridging bronchus, abortive right main bronchus, and tracheal stenosis due to absence of the tracheal pars membranacea with "ring" tracheal cartilages is described. The technique is applicable to demonstration of the anatomic features of other abnormalities of branching pattern or caliber of the trachea and major bronchi.

Bronchi↗
PubMed1990

Morphometric studies of cystic and tubulointerstitial kidney diseases with hepatic fibrosis in children.

Portal tract fibrosis with biliary ductular enlargement or proliferation occurs in a number of genetic diseases that have cystic or tubulointerstitial renal lesions. These include some with renal cystic disease such as autosomal recessive diseases (e.g., infantile polycystic disease, juvenile polycystic disease, and Meckel's syndrome), autosomal dominant diseases (e.g., adult polycystic disease) and, rarely, tuberose sclerosis and dominant glomerulocystic disease. Portal tract fibrosis with biliary enlargement and proliferation occurs also with tubulointerstitial kidney diseases. These probably include at least three disorders in the category nephronophthisis-congenital hepatic fibrosis (one autosomal recessive disease and two either autosomal or X-linked recessive diseases) plus Jeune's syndrome (the tubulointerstitial diseases Fanconi's familial nephronophthisis and anti-tubular membrane antibody disease do not regularly cause hepatic fibrosis). Morphometric data on ratios of bile ductules to connective tissue in hepatic portal tracts show high values for infantile polycystic disease (mean, 0.616) compared to lower values for juvenile polycystic disease (mean, 0.286). That the cystic renal lesions of the first two diseases differ in type and time course is known. Similar data on ratios of glomeruli plus tubules to connective tissue in renal cortices and of tubules to connective tissue in outer medullary zones of kidneys, respectively, are as follows: for Fanconi's nephronophthisis, 0.445 and 0.197; for anti-tubular basement membrane antibody disease, 0.585 and 0.164; and for the three types of nephronophthisis-congenital hepatic fibrosis studied, 0.668 and 0.446, 1.39 and 0.921, and 1.18 and 0.12. These data support clinical impressions that the category nephrophthisis-congenital hepatic fibrosis includes more than one disease entity.

Bile Ducts, Intrahepatic↗
PubMed1990

Left atrial atheromatosis in childhood nephrotic syndrome.

Three male children who had onset, at approximately age 2 years, of nephrotic syndrome, which progressed to renal insufficiency had left atrial atheromatosis at autopsy disproportionate to the degree of aortic or vascular atheromatosis found. The atrial atheromatous process was distributed in elongated nodules, which had a ridged or corduroy-like appearance on gross examination. Two of the patients showed renal lesions of advanced focal glomerulosclerosis, but one had membranoproliferative glomerulopathy, suggesting that the "syndrome" of early onset nephrotic syndrome progressing to renal insufficiency, hyperlipidemia, and exaggerated left atrial atheromatosis, of which association we have not found a specific report, is etiologically heterogeneous. The patients reported died in 1943, 1952, and 1963. Whether more recent methods of treatment of nephrotic syndrome, hyperlipidemia, or chronic renal insufficiency in children have altered the incidence of such disproportionate left atrial atheromatosis is not known.

Arteriosclerosis↗