Biomedical subjects

B K Hall

Publications and source records attributed to B K Hall.

At least 55 records · Page 3Linked to original sources

PubMed1994

Formation of cartilaginous nodules and heterogeneity in clones of HH 17 mandibular ectomesenchyme from the embryonic chick.

In vitro cloning of embryonic cells is a powerful tool for understanding the mechanism and timing of cell differentiation during development. Although in vitro mass culture of chondrogenic mesenchymal cells and clonal culture of already differentiated chondrocytes have been reported, clonal culture of chondrogenic ectomesenchymal cells at a postmigratory stage but prior to chondrogenic cell condensation has not been reported, nor have cartilage nodules been obtained in clonal culture. We cloned chick mandibular ectomesenchymal cells from HH stage 17 chick embryos. These cells produced clones that underwent chondrogenesis as determined by the presence of alcian blue-staining extracellular matrix and immunohistochemical visualization of type II collagen. Chondrogenic clones formed three-dimensional cartilaginous nodules. This postmigratory mandibular ectomesenchyme is heterogeneous, containing two different types of unipotential cells that give rise to chondrogenic and nonchondrogenic cells, plus bipotential cells that give rise to both chondrogenic and nonchondrogenic cells.

Animals↗

PubMed1994

Hypertrophy is not a prerequisite for type X collagen expression or mineralization of chondrocytes derived from cultured chick mandibular ectomesenchyme.

Meckel's cartilage in the avian mandible is a neural crest-derived permanent cartilage. To investigate whether chondrocytes that form Meckel's cartilage can be induced to undergo maturation and mineralization by manipulating the environment, we used in vitro micromass culture in which young embryonic mandibular ectomesenchymal cells were maintained at a high cell density (2 x 10(7) cells/ml) and treated with ascorbic acid (AA) or with dexamethasone and ascorbic acid (DEX + AA). Chondrogenesis and chondrocyte maturation were analyzed by histological, immunohistochemical and SDS/PAGE techniques. Chick mandibular ectomesenchymal cells from Hamburger and Hamilton (J. Morphol. 88:49-92, 1951) stage 21 (HH stage 21) chick embryos undergo chondrogenesis forming cartilage nodules when maintained under micromass culture conditions. These chondrocytes undergo maturation in response to AA but not DEX. Addition of AA to culture medium induced type X collagen expression by these chondrocytes. With prolonged culture, chondrocytes began to mineralize turning cartilage nodules into completely mineralized structures. There was no correlation between chondrocyte size and type X collagen expression. Small chondrocytes as well as large (hypertrophic) chondrocytes expressed type X collagen and then underwent mineralization. Co-treatment of cultures with DEX + AA caused reduction of chondrogenesis and inhibited chondrocyte maturation and mineralization seen with AA alone.

Animals↗

PubMed1993

A histological processing technique that preserves the integrity of calcified tissues (bone, enamel), yolky amphibian embryos, and growth factor antigens in skeletal tissue.

We have devised a processing technique to embed calcified tissues, such as bone and tooth enamel, in paraffin, to preserve the delicate antigenic sites of molecules such as growth factors. The same technique, omitting the decalcification step, allows delicate tissues, such as axolotl embryos (Ambystoma mexicanum) containing large yolk masses, to be easily handled during tissue processing and to be serially sectioned. Specimens were all fixed in periodate-lysine-paraformaldehyde (PLP) fixative at 5 degrees C. Bone and teeth were decalcified in an EDTA-G solution at -4 degrees C. Maintaining a temperature of 5 degrees C, the decalcified samples were then washed (with PBS, pH 7.2, under vacuum) to remove glycerol. Both the decalcified tissues and the yolky embryos were dehydrated through an ascending series of isopropanol and embedded in low melting-point paraffin under vacuum. Acidic fibroblast growth factor (aFGF) was located in cells of the expanded cambial layer in the early fracture calluses of male CD-1 mice, demonstrating retention of antigenic sites. The results reported here have not previously been obtained with existing processing and embedding techniques.

Ambystoma↗

PubMed1993

Expression of four growth factors during fracture repair.

Fracture repair offers an opportunity to study the physiology of bone formation at the fracture site. Isolation of growth factors from bone matrix has implicated growth factors as participants in bone physiology. We therefore examined the expression patterns of aFGF, IGF-I, PDGF, and TGF-beta during fracture repair. An animal model has been developed to study repair of tibial fractures. The model provides both reproducible and quantifiable results, allowing the fracture repair process to be divided into four stages (Bourque et al., Lab. Anim. Sci 42: 369-374, 1992). Fractured tibiae were examined immunohistochemically with polyclonal antibodies to four growth factors. PDGF was visualized in macrophages in close proximity to the periosteum during stage 1. aFGF was visualized in cells of the expanded cambial layer and was associated with a rapid increase in the population of fibroblast-like mesenchymal cells during stage 2. IGF-I was visualized in young chondroblasts at the edge of the cartilage mass replacing the fibrous callus during stage 3. TGF-beta was visualized in calcified matrix producing chondrocytes at the edge of ossification fronts penetrating the cartilage callus during stage 4. The immunohistochemical results suggest that these growth factors act as local simulators of the repair process.

Animals↗

PubMed1992

Edgeworth's legacy of cranial muscle development with an analysis of muscles in the ventral gill arch region of batoid fishes (Chondrichthyes: Batoidea).

A series of studies by Edgeworth demonstrated that cranial muscles of gnathostome fishes are embryologically of somitic origin, originating from the mandibular, hyoid, branchial, epibranchial, and hypobranchial muscle plates. Recent experimental studies using quail-chick chimeras support Edgeworth's view on the developmental origin of cranial muscles. One of his findings, the existence of the premyogenic condensation constrictor dorsalis in teleost fishes, has also been confirmed by molecular developmental studies. Therefore, developmental mechanisms for patterning of cranial muscles, as described and implicated by Edgeworth, may serve as structural entities or regulatory phenomena responsible for developmental and evolutionary changes. With Edgeworth's and other studies as background, muscles in the ventral gill arch region of batoid fishes are analyzed and compared with those of other gnathostome fishes. The spiracularis is regarded as homologous at least within batoid fishes, but its status within elasmobranchs remains unclear; developmental modifications of the spiracularis proper are evident in some batoid fishes and in several shark groups. The peculiar ventral extension of the spiracularis in electric rays and some stingrays may represent convergence, probably facilitating ventilation and/or feeding in both groups. The evolutionary origin of the "internus" and "externus" remains uncertain, despite the fact that a variety of forms of the constrictor superficiales ventrales in batoid fishes indicates an actual medio-ventral extension of the "externus." The intermandibularis is probably present only in electric rays. The "X" muscle occurs only in electric rays and is considered to be Edgeworth's intermandibularis profundus. Its association with the adductor mandibular complex in narkinidid and narcinidid electric rays may relate to its functional role in lower jaw movement. Contrary to common belief, in most batoid fishes as well as some sharks, muscles that originate from the branchial muscle plate and extend medially in the ventral gill arches do exist: the medial extension of the interbranchiales in most batoid fishes and some sharks and the "Y" muscle in the pelagic stingrays Myliobatos and Rhinoptera. The latter is another example of the medial extension of the "internus." Whether the interbranchiales and "Y" muscle are homologous within elasmobranchs and whether homologous with the obliques ventrales and/or transversi ventrales of osteichthyan fishes await further research. Four hypobranchial muscles are recognized in batoid fishes: the coracomandibularis, coracohyoideus, coracoarcualis, and coracohyomandibularis. The coracohyoideus is discrete from the coracoarcualis; its complete structural separation from the latter occurs in several groups of batoid fishes.(ABSTRACT TRUNCATED AT 400 WORDS)

Anatomy, Comparative↗

PubMed1992

The membranous skeleton: the role of cell condensations in vertebrate skeletogenesis.

Elements of the vertebrate skeleton are initiated as cell condensations, collectively termed the 'membranous skeleton' whether cartilages or bones by Grüneberg (1963). Condensations, which were identified as the basic cellular units in a recent model of morphological change in development and evolution (Atchley and Hall 1991) are reviewed in this paper. Condensations are initiated either by increased mitotic activity or by aggregation of cells towards a centre. Prechondrogenic (limb bud) and preosteogenic (scleral ossicle) condensations are discussed and contrasted. Both types of skeletogenic condensations arise following epithelial-mesenchymal interactions; condensations are identified as the first cellular product of such tissue interactions. Molecular characteristics of condensations are discussed, including peanut agglutinin lectin, which is used to visualize prechondrogenic condensations, and hyaluronan, hyaladherins, heparan sulphate proteoglycan, chondroitin sulphate proteoglycan, versican, tenascin, syndecan, N-CAM, alkaline phosphatase, retinoic acid and homeo-box-containing genes. The importance for the initiation of chondrogenesis or osteogenesis of upper and lower limits to condensation size and the numbers of cells in a condensation are discussed, as illustrated by in vitro studies and by mutant embryos, including Talpid3 in the chick and Brachypod, Congenital hydrocephalus and Phocomelia in the mouse. Evidence that genes specific to the skeletal type are selectively activated at condensation is discussed, as is a recent model involving TGF-beta and fibronectin in condensation formation. Condensations emerge as a pivotal stage in initiation of the vertebrate skeleton in embryonic development and in the modification of skeletal morphology during evolution.

Animals↗

PubMed1992

NF1-related locus on chromosome 15.

A neurofibromatosis type I (NF1)-related locus has been identified on chromosome 15. It contains a partial copy of the NF1 GAP-related domain, which is known to interact with the ras protooncogenes. However, the chromosome 15 sequence contains multiple deletions resulting in frameshift mutations and stop codons in several highly conserved sequence blocks. The locus on chromosome 15 therefore represents an NF1 pseudogene. This nonprocessed NF1 pseudogene may produce additional fragments in Southern blotting, pulsed-field gel, and PCR experiments with some NF1 cDNA probes or oligonucleotides. In addition, certain regions of the NF1 gene also cross-hybridize with a locus on chromosome 14. These loci must be considered in mutation analysis of patients with NF1 since aberrant findings may not always reflect changes in the NF1 gene.

Base Sequence↗

PubMed1992

A reproducible method for producing and quantifying the stages of fracture repair.

Male CD-1 mice, 4 to 6 months of age, were used to establish a reproducible model to study the stages of fracture repair. A custom-designed fracture apparatus was constructed, and trials with it demonstrated its capacity to reliably reproduce a closed fracture of the tibia. Dietary and sleep habits in the treated mice were the same as unfractured control mice. Four stages of fracture repair were documented and the duration of each stage was quantifiable and reproducible. The last stage of fracture repair was completed by 21 days postfracture. The reproducibility of the fracture, the reproducibility of the times and stages of fracture repair, the relatively short time to complete the fracture repair process, and the minimal discomfort which allowed the mice to maintain a normal daily routine, suggest that this is an ideal animal model for studying the fracture repair process.

Animals↗

PubMed1991

Toward an understanding of the epithelial requirement for osteogenesis in scleral mesenchyme of the embryonic chick.

Explants of scleral tissue from chick embryos of H.H. stage 29-36 (6-10 days of incubation) were used to determine if the epithelial-mesenchymal interaction which initiates scleral bone formation is cell contact, extracellular matrix, or diffusion mediated. Transfilter tissue recombinations, in which explanted interacting tissues are associated across interposing Nuclepore filters of various pore sizes and thicknesses, were performed with scleral mesenchyme and epithelium. When filters with pore sizes which would allow the passage of cell processes and diffusible substances were used, osteogenesis was initiated in the scleral mesenchyme. When cell processes were blocked with thicker filters or smaller pore sizes, bone formation still occurred, indicating that a diffusible substance mediates this tissue interaction. Further support for a diffusion-mediated interaction came from transfilter experiments using dialysis membranes to discriminate the size of the molecule(s), and Millipore filters to determine the distance over which these molecules travel. These experiments revealed that the scleral epithelial diffusible factor has a molecular weight of between 3500 and 6000 daltons, and acts over distances between 150 and 300 microns.

Allantois↗

PubMed1991

On the importance of cAMP and Ca++ in mandibular condylar growth and adaptation.

The origin of the mandibular condylar cartilage is not periosteal, like that of the other secondary cartilages; this cartilage originates in a cellular blastema of its own. Despite the fact that the development of secondary cartilages, in general, is dependent on mechanical irritation, that of the condylar cartilage is not. The low level of function experienced postnatally seems to favor growth, but because the proliferation cells of the condylar cartilage are multipotential, they switch their differentiation pathway in the direction of osteoblasts in the absence of function, and growth of the cartilage ceases. This regulation of differentiation is mediated by maturation of the cartilage cells. If function is not present, maturation advances rapidly, and the mature cartilage induces bone formation instead of cartilage. Cyclic AMP and Ca are important mediators in this process, because they affect the advancement of maturation.

Animals↗

PubMed1991

The nature of the epithelium in acquired cholesteatoma.

Monoclonal antibodies with defined specifications for individual cytokeratins were used to stain the epithelia of the external auditory meatus, the middle ear and cholesteatoma. The observed staining indicated that the epithelium of the external auditory meatus has a pattern of keratin expression typical of epidermis in general and the epithelium of the middle ear resembles simple columnar epithelia. The pattern of staining of cholesteatoma closely resembled that of the skin of the external auditory meatus.

Antibodies, Monoclonal↗

PubMed1991

Polymerase chain reactions with alphoid-repeat primers in combination with Alu or LINEs primers, generate chromosome-specific DNA fragments.

Y alphoid primers in combination with Alu and LINEs primers generated new DNA fragments in polymerase chain reactions (PCR) on DNA from a Y-only somatic cell hybrid but not from X-only, 3-only, or 21-only hybrids. X alphoid primers used in a similar manner generated new DNA fragments from the X-only hybrid, and 1 of the primers (X2) also generated new DNA fragments on 3-only and 21-only hybrids when used in conjunction with Alu or LINEs primers. In all but one case, consensus alphoid primers generated new chromosome-specific fragments in PCR reactions with the Alu or LINEs primers. A search for cryptic Alu- or alphoid-alone PCR products as the source for one Alu-alphoid band (chosen at random) was negative. Partial sequencing of products demonstrated that alphoid and Alu sequences were indeed contiguous in some newly synthesized DNA fragments. While Alu or LINEs primers generate smears of DNA fragments on total human DNA, the alphoid-non-alphoid repeat combinations generated electrophoretically distinguishable bands of DNA when the template was total DNA. While these were distinguishable with different chromosome-specific alphoid primers, the DNA fragments were not of the same sizes as those generated with the chromosome-only hybrids.

Animals↗

PubMed1991

A model for development and evolution of complex morphological structures.

How 'complex' or composite morphological structures like the mammalian craniomandibular region arise during development and how they are altered during evolution are two major unresolved questions in biology. Herein, we have described a model for the development and evolution of complex morphological structures. The model assumes that natural selection acts upon an array of phenotypes generated by variation in a variety of underlying genetic and epigenetic controlling factors. Selection refines the integration of the various morphogenetic components during ontogeny in order to produce a functioning structure and to adapt the organisms to differing patterns of environmental heterogeneity. The model was applied to the development and evolution of the mammalian mandible (which is used as a paradigm of complex morphological structures). The embryology of the mandible was examined in detail in order to identify the fundamental developmental units which are necessary to assemble the final morphological structure. The model is quite general since equivalent units exist for the development of many other biological structures. This model could be applied to many other developing morphological structures as well as other groups of organisms. For example, it can be applied to cell parameters during Drosophila development (Atchley, 1987). The model as discussed in this paper assumes that morphological changes in the mandible result from evolutionary changes in its underlying developmental units. The developmental units relate to characteristics of cellular condensations which are produced from the differentiation of embryonic neural crest cells. The developmental units include: the number of stem cells in preskeletal condensations (n), the time of initiation of condensation formation (t), the fraction of cells that is mitotically active within a condensation (f), the rate of division of these cells (r), and their rate of cell death (d). These units and their derivative structures are discussed in terms of types of tissue differentiation (chondrogenesis, osteogenesis, primary/secondary osteogenesis, intramembranous/endochondral ossification) and growth properties of major morphological regions of the mandible. Variation in these five units provides the developmental basis for ontogenetic and phylogenetic modification of mandibular morphology. We have discussed how these developmental units are influenced by (a) the cell lineage from which they arise, (b) epithelial-mesenchymal (inductive tissue) interactions, (c) regulation of cell differentiation, and (d) extrinsic factors such as muscles, teeth and hormones. Evidence was provided that variation in mandibular morphology is heritable, subject to modification by natural selection, and that divergence among different genetic stocks has apparently occurred through changes in these developmental units and their derivative structures.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Effects of growth factors on the differentiation of neural crest cells and neural crest cell-derivatives.

During neurulation, neural crest cells migrate to many regions of the body to give rise to a wide variety of cell types. Many premigratory neural crest cells are pluripotent, their potency for differentiation being gradually restricted as they migrate along definite pathways and interact with factors present in the microenvironment. Effects of growth factors on these cells have been discussed in the present review. Mediation of growth factors in differentiation varies with the cell type. Growth factors exert a direct influence on the differentiation of neural and other related neural crest-derived tissues such as endocrinal tissues but evidence for such influences on neural crest-derived mesenchymal tissues is limited. For example, NGF, BDNF, and other factors present in neural tube extracts and glioma cell conditioned medium are essential for the differentiation of sensory neurons. Similarly, NGF, insulin, IGFs and possibly other undescribed factors are necessary for the differentiation of sympathetic neurons. IGFs also enhance the proliferation of mesenchymal derivatives of both neural crest and mesodermal origin. Glucocorticoid-mediated differentiation of neural crest-derived chromaffin endocrine cells that are ontogenetically closely related to sympathetic neurons can be inhibited by NGF, and chromaffin cells can be induced to express the neuronal phenotype by NGF. Some growth factors, such as NGF, act on neural crest- and not on placodally-derived neurons, whether the former are sensory or sympathetic. Placodal sensory neurons possess NGF receptors, but only display a limited response to NGF, perhaps because of low affinity of the receptors. Other growth factors, such as BDNF, selectively act upon sensory neurons, whether neural crest- or placodally-derived. Although extracellular matrix products play a role in initiating the differentiative process, signals from growth factors are necessary for the establishment of the functionally competent phenotype of neural crest-derived neurons, a situation that does not apply for neural crest-derived mesenchymal cells. It is interactions with ECM components deposited by epithelia that govern the differentiation of mesenchymal derivatives. Growth factors do effect proliferation of mesenchymal derivatives and inhibit mesenchymal differentiation. Although direct involvement of single growth factors in transformation o f one mesenchymal phenotype to another has not been reported so far, their localization at sites of epithelial-mesenchymal interactions in palate teeth and mandible, and the ability of excess growth factors to interrupt normal development is suggestive of their possible involvement. One group of growth factors, BMPs, can influence differentiation of cartilage, including those of neural crest origin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Localization of the translocation breakpoint in a female with Menkes syndrome to Xq13.2-q13.3 proximal to PGK-1.

Menkes syndrome is a rare X-linked recessive disorder characterized by an inability to metabolize copper. A female patient with both this disease and an X; autosome translocation with karyotype 46,X,t(X;2)(q13;q32.2) has previously been described. The translocation breakpoint in Xq13 coincides with a previous assignment of the Menkes gene at Xq13 by linkage data in humans and by analogy to the mottled mutations which are models for Menkes disease in the mouse. Therefore, this translocation probably interrupts the gene for Menkes syndrome in band Xq13. We describe here experiments to precisely map the translocation breakpoint within this chromosomal band. We have established a lymphoblastoid cell line from this patient and have used it to isolate the der(2) translocation chromosome (2pter----2q32::Xq13----Xqter) in human/hamster somatic cell hybrids. Southern blot analyses using a number of probes specific for chromosomes X and 2 have been studied to define precisely the location of the translocation breakpoint. Our results show that the breakpoint in this patient--and, therefore, likely the Menkes gene--maps to a small subregion of band Xq13.2-q13.3 proximal to the PGK1 locus and distal to all other Xq13 loci tested.

Animals↗

PubMed1990

Tissue interactions involving cranial neural crest in cartilage formation in Xenopus laevis (Daudin).

Deletion experiments in neurula stage embryos of Xenopus laevis provide an approximate anuran fate map of the chondrogenic cranial neural crest which is similar to maps produced for other vertebrates. Crest cells in the transverse (rostral) neural fold do not contribute to the skeleton; other cranial crest cells contribute to the larval cranial and visceral skeletons in a rostral to caudal sequence. Grafting experiments show that contact with stomodeal (pharyngeal) endoderm is necessary to elicit chondrogenesis in cranial neural crest. Crest cells in the transverse neural fold, which do not normally form cartilage, formed cartilage in grafts, indicating that they do have the potential to form cartilage.

Animals↗

PubMed1990

Paralysis and growth of the musculoskeletal system in the embryonic chick.

Avian embryos can be completely paralyzed by injection of neuromuscular-blocking agents. We used a single injection of decamethonium iodide to paralyze embryos at 7, 8, or 10 days of incubation and analyzed the growth of individual bones (clavicle, mandible, ulna, femur, tibia, humerus) and of individual muscles that act upon some of those bones (clavicular and sternal heads of m. pectoralis, and mm. biceps brachii, depressor mandibulae, pseudotemporalis, and adductor externus). Growth of the bones is not equally affected by paralysis. Only 27% of clavicular growth (by mass) but 77% of mandibular growth occurred in paralyzed embryos, whereas the four long bones exhibited 52-63% of their normal growth. Analysis of muscle weight, fiber length and physiological cross-sectional area (weight/fiber length) indicate that there was greater reduction of the muscles acting on the limbs than of those acting on the mandible, i.e., diminished growth of the skeleton is correlated with reduced muscular activity. Specific retardation of clavicular growth is due to fusion of sternal rudiments and collapse of the thorax, as well as virtual absence of the musculature that normally attaches to the clavicle. We discuss these results in the light of intrinsic and extrinsic factors governing growth of the embryonic skeleton. Paralysis reduces skeletal growth by reducing both the movements taking place in ovo, and the loads imposed on the bones by muscle contraction, changes that represent alterations in the mechanical environment of the skeleton.

Animals↗

PubMed1990

Development and evolutionary origins of vertebrate skeletogenic and odontogenic tissues.

This review deals with the following seven aspects of vertebrate skeletogenic and odontogenic tissues. 1. The evolutionary sequence in which the tissues appeared amongst the lower craniate taxa. 2. The topographic association between skeletal (cartilage, bone) and dental (dentine, cement, enamel) tissues in the oldest vertebrates of each major taxon. 3. The separate developmental origin of the exo- and endoskeletons. 4. The neural-crest origin of cranial skeletogenic and odontogenic tissues in extant vertebrates. 5. The neural-crest origin of trunk dermal skeletogenic and odontogenic tissues in extant vertebrates. 6. The developmental processes that control differentiation of skeletogenic and odontogenic tissues in extant vertebrates. 7. Maintenance of developmental interactions regulating skeletogenic/odontogenic differentiation across vertebrate taxa. We derive twelve postulates, eight relating to the earliest vertebrate skeletogenic and odontogenic tissues and four relating to the development of these tissues in extant vertebrates and extrapolate the developmental data back to the evolutionary origin of vertebrate skeletogenic and odontogenic tissues. The conclusions that we draw from this analysis are as follows. 8. The dermal exoskeleton of thelodonts, heterostracans and osteostracans consisted of dentine, attachment tissue (cement or bone), and bone. 9. Cartilage (unmineralized) can be inferred to have been present in heterostracans and osteostracans, and globular mineralized cartilage was present in Eriptychius, an early Middle Ordovician vertebrate unassigned to any established group, but assumed to be a stem agnathan. 10. Enamel and possibly also enameloid was present in some early agnathans of uncertain affinities. The majority of dentine tubercles were bare. 11. The contemporaneous appearance of cellular and acellular bone in heterostracans and osteostracans during the Ordovician provides no clue as to whether one is more primitive than the other. 12. We interpret aspidin as being developmentally related to the odontogenic attachment tissues, either closer to dentine or a form of cement, rather than as derived from bone. 13. Dentine is present in the stratigraphically oldest (Cambrian) assumed vertebrate fossils, at present some only included as Problematica, and is cladistically primitive, relative to bone. 14. The first vertebrate exoskeletal skeletogenic ability was expressed as denticles of dentine. 15. Dentine, the bone of attachment associated with dentine, the basal bone to which dermal denticles are fused and cartilage of the Ordovician agnathan dermal exoskeleton were all derived from the neural crest and not from mesoderm. Therefore the earliest vertebrate skeletogenic/odontogenic tissues were of neural-crest origin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗