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Biomedical subjects

B K Hall

Publications and source records attributed to B K Hall.

At least 127 records · Page 7Linked to original sources
PubMed1979

Lack of association between avian cartilages of different embryological origins when maintained in vitro.

The possibility that cartilages of differing embryological origins behave as separate types with respect to cell-to-cell associations was tested by placing the cut ends of transversely sectioned embryonic chick tibial cartilages (of mesodermal origin) in apposition to transversely sectioned Meckel's cartilages (neural crest (ectodermal) cartilage) on the surface of a semi-solid organ culture medium and maintaining the combinations in vitro for five to ten days. Tibia-tibia and Meckel's cartilage-Meckel's cartilage (homotypic) combinations, which served as controls, became united by a common extracellular matrix and by the proliferation of chondroblasts. Analysis of combinations where one partner had been prelabelled with 3H-thymidine indicated that chondroblasts intermingled at the contact zone. In contrast, tibia-Meckel's cartilage (heterotypic) combinations became separated by a layer of fibrous tissue. The chondroblasts at the contact zone failed to intermingle. We conclude that avian embryonic chondrocytes are not all equivalent and that part of their nonequivalence could be related to their embryological origin either from the mesoderm or from the ectodermal neural crest.

Animals↗
PubMed1979

Ability of neural crest cells from the embryonic chick to differentiate into cartilage before their migration away from the neural tube.

Whether neural crest cells from the avian embryo are determined for chondrogenesis before they begin their migration away from the neural tube (i.e., before H. H. stages 8.5--9) was investigated by establishing neural folds from embryos of H. H. stages 5--11 either in organ culture, or as grafts to the chorioallantoic membranes of host embryos. Cartilage differentiated from neural folds taken from embryos of H. H. stages 5--7 but not from those taken from older embryos. This stage specific pattern was reversed when the tissue adjacent to the neural tube was grafted to the chorioallantoic membrane. Cartilage only formed from tissues isolated later than H. H. stage 8; i.e., when these adjacent tissues contain neural crest cells. We concluded that neural crest cells are determined for chondrogenesis while still in the neural tube and before their migration to the face and head. This is in contrast to the situation in the only other group which has been examined, the urodele amphibians.

Animals↗
PubMed1979

The timing of the onset of osteogenesis in the tibia of the embryonic chick.

Haematoxylin, Alcian Blue-Chlorantine Fast Red (ABCR) and the Ralis osteoid-specific stain were employed to closely follow the histogenesis of the tibia of the embryonic chick so as to provide an accurate description of the onset of ossification. An overview of the major cytological events preceding osteogenesis in the tibia was obtained from hindlimbs of embryos of H. H. (Hamburger and Hambilton, '51) stages 16-26 (2.5-5 days of incubation) stained with ABCR. A description of the cytological changes in the periosteum as it develops from the perichondrium and an analysis of the timing of the onset of osteoid deposition was obtained from the tibiae of accurately aged and staged embryos of H. H. stages 28-32 (5.5-8 days). These tibiae were stained specifically for the detection of osteoid: the freshly-secreted, unmineralized product of fully-differentiated osteoblasts. The perichondrium transformed into a bi-layered periosteum at H. H. late stage 29 (6.5 days) while osteoid was first detected adjacent to the hypertrophic cartilage of H. H. stage 30 (6.5-7 days) tibial diaphyses. These results, correlated with the immunoflourescent studies of Von der Mark et al. ('76a,b), which revealed the presence of Type I (bone-type) collagen-synthesizing cells in the perichondria of tibiae from embryos of H. H. stage 28 (5.5-6 days), demonstrated that the onset of determination of cells for osteogenesis and the cytodifferentiation of the periosteum are not temporally coupled.

Animals↗
PubMed1979

Selective proliferation and accumulation of chondroprogenitor cells as the mode of action of biomechanical factors during secondary chondrogenesis.

Secondary cartilage fails to differentiate on membrane bones of embryonic chicks which have been paralyzed by the in ovo injection of D-tubocurarine chloride at ten days of incubation. A planimetric analysis of serial sections of a membrane bone (the quadratojugal) from control (mobile), and from paralyzed embryos, indicated that osteogenesis was not slowed in paralyzed embryos. However the rate of accumulation of periosteal progenitor cells was significantly lower in paralyzed than in mobile embryos. Quantitative analysis of 3H-thymidine-labelled progenitor cells indicated that the slowed accumulation of progenitor cells was the result of fewer progenitor cells initiating DNA synthesis and mitosis. Between 10 and 11 days of incubation, 60 to 75 more 3H-thymidine-labelled progenitor cells accumulated in mobile embryos than accumulated on each quadratojugal in paralyzed embryos. This subpopulation of cells could represent the chondroprogenitor cells which produce secondary cartilage in mobile embryos. If this is so, then biomechanical factors control the ability of the embryo to produce secondary cartilage by allowing the selective accumulation of chondrogenic progenitor cells.

Animals↗
PubMed1979

Retention during embryonic life of the ability of avian spinal cord to induce somitic chondrogenesis in vitro.

It is well established that the spinal cord of embryonic vertebrates induces sclerotomal somitic mesoderm to chondrify. We have investigated whether the spinal cord retains this inductive ability for the duration of the life of the avian embryo. Somites were isolated from embryos of H.H. stages 16 to 18 and either cultured alone in a medium which would not allow spontaneous chondrogenesis or cultured in direct contact with the spinal cord from embryos ranging in age between H.H. stages 33 and 44 (7 1/2--18 days of incubation). Somites cultured alone did not chondrify. Somites cultured in contact with either the ventral surface of the spinal cord or with the ependyma of the spinal cord chondrified in virtually 100% of all cultures--irrespective of the age of the donor embryo providing the spinal cord. The somites which were cultured in contact with the dorsal surface of the spinal cord did not undergo chondrogenesis. We conclude that the ventral spinal cord and the ependyma retain inductive ability through embryonic life and discuss the possible reasons for this.

Animals↗
PubMed1978

Use of the L-proline analog, L-azetidine-2-carboxylic acid (LACA) to analyse embryonic growth and determination and expression of the chondrogenic phenotype in vivo and in vitro.

The L-proline analog, L-azetidine-2-carboxylic acid, (LACA) was injected into embryonated eggs of the common fowl, Gallus domesticus at daily doses of 350 microgram/egg on one or several days betweeh 8 and 12 days of incubation. Treatment at nine-days of incubation preferentially retarded embryonic growth to the twelfth day but recovery of growth rate occurred by 15 days of incubation. Relationships between growth and LACA-inhibited aspects of collagenogenesis are discussed. The earliest aged embryos from which isolated stem cells from membrane bones will form secondary cartilage is ten days of incubation. Secondary chondrogenesis on the quadratojugal, a membrane bone of the skull, was inhibited by treatment of whole embryos with LACA at nine days of incubation but not by treatment at eight days. We concluded that an event involving collagen began at nine days of incubation, was blocked by LACA and was part of the process of chondrogenic determination of these stem cells. Addition of LACA to the medium in which already determined stem cells from the quadratojugal were cultured prevented expression of the chondrogenic phenotype. This proline analog is then a useful probe for events relating both to determination and to expression of the differentiated state, and allows conclusions to be drawn regarding the role of collagenogenesis in these events.

Animals↗
PubMed1977

Thallium-induced achondroplasia in chicken embryos and the concept of critical periods during development.

Achondroplasia was induced in chicken embryos by in ovo application of 0.6 mg/egg thallium sulfate. The critical (sensitive) period for production of achondroplasia began on day 5 of incubation and ended at the start of HH stage 35 (8.5 days). The end of the critical period was accurately timed and found to be 205-207 hours of incubation and to coincide with a 66% decrease in growth rate of the embryos. Treatment resulted in reduced tibial growth one day later, tibial angulation two days later, and chrondrocytic necrosis four days later. The last was therefore not the cause of the angulation. Tibias were taken from thallium-treated and control donor embryos of various ages and grafted to the chorioallantoic membranes of treated and control host embryos of various ages during and outside the critical period and achondroplastic changes induced in grafted tibias exposed to thallium while on the chorioallantoic membrane. The critical period was extended into day 10 of incubation in such grafted tibias. Tibias maintained for seven days in organ culture were achondroplastic if pretreated with thallium at seven or eight days of incubation but not at ten days. Exposure of as little as 0.5 hour was sufficient to elicit micromelia when the tibias were grafted or organ cultured. Thallium therefore rapidly binds to skeletal tissues during a critical period of embryonic development but this critical period may be extended when tibias are removed from the embryo.

Abnormalities, Drug-Induced↗
PubMed1976

The use of variable lactate/malic dehydrogenase ratios to distinguish between progenitor cells of cartilage and bone in the embryonic chick.

The activities of LDH and MDH have been studied, both in differentiated cartilage and bone from the embryonic chick, and in the pool of mixed osteogenic and chondrogenic stem cells found on the quadratojugal, a membrane bone. In confirmation of the model proposed by Reddi & Huggins (1971) we found that the LDH/MDH ratio was greater than 1 in cartilage and less than 1 in bone. Furthermore we established, for the first time, that ratios occurred in the chondrogenic and osteogenic stem cells, similar to the ratios in their differentiated counterparts. Alteration in LDH/MDH resulted from variations in the level of LDH/mug protein. MDH/mug protein remained constant, even when LDH/MDH was changing. We interpret these results in terms of adaptation of chondrogenic progenitor cells for anaerobic metabolism and anticipate that our model will be applicable to other skeletal systems where stem cells are being studied.

Age Factors↗
PubMed1975

The repair of fractured membrane bones in the newly hatched chick.

Repair of a fractured membrane bone, the quadratojugal (QJ), has been studied in the newly hatched chick. Complete open fractures never united by bony fusion, even in birds maintained for six months post-fracture. Extraperiosteal connective tissue invaded the fracture gap and formed thick fibrous bundles which stabilised the fracture. Cartilage of two types formed on these bones. One was derived from periosteal cells and the other from osteoblasts or osteocytes. Considerably more cartilage formed in bones partially fractured than in those completely fractured. The "periosteal" cartilage did not form if the periosteum was removed at the time the bone was fractured. This was because, although the fibrous layer of the periosteum regenerated, the cambial layer did not. Metaplastic cartilage did form in the absence of the periosteum. Isolating fractured bones within polyethlene or glass tubes prevented accumulation of a blastema between the bony fragments. Cartilage did not form inside the tubes but did form where the ends of the tubes abutted onto the bones. Large defects in the bones (4 mm gaps, 4 mm of bone in the place of the QJ) healed via fibrous union with minimal osteogenesis and no chondrogenesis. Severing M. depressor mandibulae at the time the bone was fractured inhibited chondrogenesis, favoured osteogenesis and resulted in development of a pseudarthrosis. The potential for differentiation of the cells of the QJ and the role of the adjacent tissues as they related to repair of the fracture was discussed, and the ability of cells from membrane bones to become chondrogenic emphasized.

Animals↗
PubMed1975

A simple, single-injection method for inducing long-term paralysis in embryonic chicks, and preliminary observations on growth of the tibia.

A method for inducing paralysis in embryonic chicks is described. This involves single injections of the neuromuscular blocking agents, D-tubocurrarine Chloride or decamethonium iodide, into 10-day embryos. The dose which optimises survival and paralysis is determined along with the effect of the drugs on embryonic growth. Decamethonium iodide at a dose of 1 mg per embryo gave maximum survival and paralysis to 18 days of incubation. Paralysis was assessed by observation of treated embryos in ovo and by examination of embryos removed from their shells between 11 and 18 days of incubation. Embryos were completely paralysed 24 hours post-injection and remained paralysed until 18 days of incubation. Paralysed embryos failed to hatch. Development of the leg musculature was severely retarded in paralysed embryos. This method of inducing paralysis has considerable advantages over previous continuous infusion methods. The growth and collagen content of the tibia in the paralysed embryos was reduced and these results, and other applications of the method, are discussed.

Acetylcholinesterase↗
PubMed1975

The origin and fate of osteoclasts.

Despite intensive and ingenious investigation, the origins and ultimate fate of the osteoclast remain shrouded in mystery. This brief review evaluates some of the recent experimental approaches used in the study of the osteoclast, especially whether they form from intra- or extra-skeletal progenitor cells, whether from the same osteoprogenitor cell as the osteoblast, and whether, once formed, they may modulate to osteoblasts. That osteoprogenitor cells can, and do, become osteoclasts is well founded, as is the conclusion that such progenitor cells originate as blood-borne, extra-skeletal cells. Evidence that sessile, intra-skeletal, progenitor cells can form osteoclasts is less direct. There is good evidence that osteoclasts both shed and take-up nuclei, but no direct evidence that nuclear shedding is accompanied by death of the osteoclast, and no direct evidence for the fate of the shed nuclei. Whether the same osteoprogenitor cell can produce either an osteoblast or an osteoclast also remains an open question.

Animals↗