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A Crawley

Publications and source records attributed to A Crawley.

30 records · Page 2Linked to original sources
PubMed1993

Quantitative evaluation of several partial Fourier reconstruction algorithms used in MRI.

Partial Fourier reconstruction algorithms exploit the redundancy in magnetic resonance data sets so that half of the data is calculated during image reconstruction rather than acquired. The conjugate synthesis, Margosian, homodyne detection, Cuppen and POCS algorithms are evaluated using spatial frequency domain analysis to show their characteristics and where limitations may occur. The phase correction used in partial Fourier reconstruction is equivalent to a convolution in the frequency domain and the importance of accurately implementing this convolution is demonstrated. New reconstruction approaches, based on passing the partial data through a phase correcting, finite impulse response (FIR), digital filter are suggested. These FIR and MoFIR algorithms have a speed near that of the Margosian and homodyne detection reconstructions, but with a lower error; close to that of the Cuppen/POCS iterative approaches. Quantitative analysis of the partial Fourier algorithms, tested with three phase estimation techniques, are provided by comparing artificial and clinical data reconstructed using full and partial Fourier techniques.

Algorithms↗
PubMed1992

Hox-4 gene expression in mouse/chicken heterospecific grafts of signalling regions to limb buds reveals similarities in patterning mechanisms.

The products of Hox-4 genes appear to encode position in developing vertebrate limbs. In chick embryos, a number of different signalling regions when grafted to wing buds lead to duplicated digit patterns. We grafted tissue from the equivalent regions in mouse embryos to chick wing buds and assayed expression of Hox-4 genes in both the mouse cells in the grafts and in the chick cells in the responding limb bud using species specific probes. Tissue from the mouse limb polarizing region and anterior primitive streak respecify anterior chick limb bud cells to give posterior structures and lead to activation of all the genes in the complex. Mouse neural tube and genital tubercle grafts, which give much less extensive changes in pattern, do not activate 5'-located Hox-4 genes. Analysis of expression of Hox-4 genes in mouse cells in the grafted signalling regions reveals no relationship between expression of these genes and strength of their signalling activity. Endogenous signals in the chick limb bud activate Hox-4 genes in grafts of mouse anterior limb cells when placed posteriorly and in grafts of mouse anterior primitive streak tissue. The activation of the same gene network by different signalling regions points to a similarity in patterning mechanisms along the axes of the vertebrate body.

Animals↗
PubMed1991

Position-dependent expression of two related homeobox genes in developing vertebrate limbs.

Many genes that control pattern formation in insects contain a conserved homeobox region which encodes a domain involved in DNA binding. One approach to understanding pattern formation in vertebrates is to examine the role of homeobox-containing genes in the developing limb. Two such genes, Hox-7.1 and Hox-8.1, are expressed in distal mesoderm, but not in the proximal core, of mouse forelimb (refs 3, 4, and D.R.D., manuscript in preparation). The proximodistal cartilage pattern in the chick wing is progressively determined in the distal mesoderm, which is maintained as a 'progress zone' by the overlying apical ectodermal ridge. Indeed, proximal cells are reprogrammed to form distal structures when placed in the progress zone and we therefore expect that genes involved in controlling limb pattern should be activated in such grafts. We tested this requirement for Hox-7.1 and Hox-8.1 in mouse limb mesoderm placed in chick wing buds. Our results reported here indicate that both genes are rapidly activated by a signal from the apical ectoderm. These properties, taken with the DNA-binding properties of the homeodomain, strongly suggest that Hox-7.1 and Hox-8.1 have fundamental roles in limb-pattern formation.

Animals↗
PubMed1990

The behaviour of cells from the distal tips of quail wing buds when grafted back into chick wings after micromass culture.

In high density culture, cells from distal tips of developing limb buds differentiate into a continuous cartilage sheet, rich in type II collagen. When grafted back into limb buds, cells cultured for a short time differentiate into cartilage and a wide range of other connective tissues, whereas cells taken from older cultures give rise only to cartilage and perichondrium. Grafts placed distally give rise to more cell types than grafts placed proximally. The results strongly suggest that chondrogenesis in culture is the result of removing the signals that pattern differentiation within the limb bud.

Animals↗
PubMed1989

Retinoic acid application to chick wing buds leads to a dose-dependent reorganization of the apical ectodermal ridge that is mediated by the mesenchyme.

Local application of retinoic acid to wing buds of chick embryos leads to dose- and position-dependent changes in the pattern of cellular differentiation. Early effects of retinoid treatment on the apical ectodermal ridge coordinate pattern changes and morphogenesis. The length of the apical ridge increases when additional digits will form but decreases when digits are lost. These changes in length can be understood in terms of a threshold response to the local retinoid concentration that results in either disappearance or maintenance of the ridge (Lee & Tickle, J. Embryol. exp. Morph. 90, 139-169 (1985)). Here, we have analysed the mechanisms involved in ridge disappearance by locally applying retinoic acid to the apex of stage 20 chick wing buds. With this treatment regime, low doses give duplicated digit patterns and higher doses truncations. The height of the apical ridge is progressively reduced with increasing doses of retinoid and the time course of ridge flattening indicates that the height of the ridge is correlated with bud outgrowth. With high doses of retinoic acid, the typical ridge, a pseudostratified epithelium in which the columnar cells are tightly packed, disappears and the epithelium at the tip of the bud consists of loosely packed cuboidal cells. Shortly after treatment, there is a decrease in the number of gap junctions between ridge cells. This early change in cell contacts suggests that gap junctions may be involved in maintaining epithelial morphology. When treated epithelium is recombined with untreated mesenchyme, an apical ridge is reestablished and distal structures can be generated. In contrast, when treated mesenchyme is recombined with the epithelium from normal buds, only proximal structures are formed. Therefore, retinoids can lead to a reorganization of the apical ectodermal ridge which is mediated and maintained by the mesenchyme.

Animals↗
PubMed1984

Analysis of upper beak defects in chicken embryos following with retinoic acid.

Implanting inert carriers soaked in retinoic acid into the anterior margin of the developing limb of chicken embryos leads to orofacial malformations as well as affecting pattern formation in the limb. Using anion-exchange beads as carriers, and soaking solutions of 1-10 mg/ml retinoic acid, almost 100% of the embryos have malformations of the face. The effects on the treated limbs range from symmetrical patterns of duplicated digits (maximum number of digits being four) to truncations in which no digits were formed at all. Typically, in the malformed faces the upper beak is completely absent, no nostrils are present and the front of the face forms a scalloped rim of tissue above the mouth. By reference to normal beak development, the seven bulges of tissue that make up the rim can be identified as derivatives of the masses of tissue that normally would fuse to form the upper beak. The roof of the mouth consists of three bulges of tissue flanked by widely separated palatal shelves. The defect can thus be classified as severe bilateral clefting of the primary palate. By examining the morphology of the faces of treated embryos, the origin of the defect can be traced to failure of the frontonasal mass to enlarge. Thus, the oronasal fissures are very wide and fusion across them to form the primary palate cannot occur. The way in which retinoic acid brings about the defect is discussed in relation to possible mechanisms involved in the production of cleft palate. The parallel is noted between the associated effects of retinoic acid on beak and limb morphogenesis and the chick mutation cpp, that also affects both face and limbs.

Abnormalities, Drug-Induced↗
PubMed1979

Survival of cells implanted in the embryonic chick limb bud: a difference between normal and malignant rat brain cells.

Cells from normal rat brain tissue did not survive and few cells could be found 1 d after grafting. In contrast, cells from a glioma and a carcinogen-treated rat brain survived well and many mitoses were observed. These malignant cells also invaded the limb. The behaviour of normal and malignant cells was followed at shorter times after grafting and some invasion by the normal cells was detected. The first signs of degeneration of normal cells were apparent around 7 h after grafting, and after this the grafts progressively deteriorated. These results support the ideal that the ability of cells to survive and grow in embryonic tissues is a characteristic of malignant cells. The findings are discussed in relation to mechanisms of tumour formation.

Animals↗
PubMed1979

Infiltration and survival: the behaviour of normal, invasive cells implanted to the developing chick wing.

The invasiveness of mouse lymphocytes and thymocytes, rabbit peritoneal neutrophil granulocytes (PMNs), mouse peritoneal macrophages (both activated and non-activated) and pig endothelial cells was assayed by implanting these cells to the chick wing bud. Cells of each type moved into the wing mesenchyme, although activated macrophages invaded poorly. PMNs were the most invasive cells and had moved well into the limb after only a few hours. PMNs, lymphocytes and thymocytes were ingested by wing mesenchyme cells. Endothelial cells, however, ingested chick blood cells. The implanted cells showed differences in ability to survive in the limb: PMNs disappeared rapidly, lymphocytes and thymocytes sometimes persisted for 24 h, while grafts of macrophages and endothelial cells were present at 24 h. Mechanisms which might be involved in the invasiveness of these cells, and also in their different abilities to survive in the chick wing, are discussed with particular reference to the production of plasminogen activator.

Animals↗
PubMed1978

Cell movement and the mechanism of invasiveness: a survey of the behaviour of some normal and malignant cells implanted into the developing chick wing bud.

A survey of the behaviour of a variety of normal and malignant tumours and cells has been carried out to gain insights into the mechanisms of tumour invasiveness. The tumours and cells were implanted into the developing chick wing bud, which is a loose mesenchyme bounded by ectoderm. The distribution of the grafted cells was examined histologically after one or two days. The special feature of this assay is that the behaviour of cells is tested in a 3-dimensional tissue. Cells from 3 different carcinomas, mouse lung tumour, rat bladder tumour and human breast tumour did not invade the mesenchyme, whereas trophoblast, sarcoma 180, cultured hamster fibroblasts (BHK, PyBHK, Nil 8, HSV Nil 8) and neuroblastoma cells did. Cells from embryonic pigmented retina and heart ventricle were non-invasive. These results suggest that cell movement may not be a common feature of all invasive tumours. The cells that did move into the mesenchyme appeared to do so by various mechanisms. Lack of contact inhibition of movement, although probably involved in the invasiveness of sarcoma 180 cells, does not appear to be necessary for invasion: cells that have been shown to exhibit contact inhibition of movement (BHK and PyBHK) also invade. Both normal and transformed cells (BHK and PyBHK; Nil 8 and HSV Nil 8) moved into the mesenchyme. Other invading cells, such as trophoblast, neuroblastoma and to a small extent, HSV Nil 8 cells, destroy the adjacent host tissue and this may be important in the invasiveness of these cells. The patterns of invasion and interactions with the host tissue were varied. Trophoblast and the fibroblasts were often elongated along the basement membrane at the ectoderm/mesenchyme border and also closely apposed to the endothelial linings of blood vessels. Sarcoma 180 and neuroblastoma cells clustered around nerves. The embryonic tissues and neuroblastoma cells were often associated with blood vessels. These results are discussed in relation to tumour invasion. A striking finding was that the carcinoma cells were frequently found positioned within the wing ectoderm on the basement membrane. This affinity of carcinoma cells for the epithelium rather than the mesenchyme leads to a reappraisal of the mechanisms involved in the invasiveness of carcinomas.

Animals↗
PubMed1978

Mechanisms of invasiveness of epithelial tumours: ultrastructure of the interactions of carcinoma cells with embryonic mesenchyme and epithelium.

Three different kinds of carcinoma cell, human breast tumours, mouse lung tumour and rat bladder tumours have been implanted into the developing chick wing to assay their invasive behaviour. We found that the majority of the carcinoma cells did not invade the mesenchyme but were positioned in the ectoderm. We examined the ultrasturcture of the interaction of the carcinoma cells with both the ectoderm and the mesenchyme to see if there are any differences. We found no specialized adhesive junctions between carcinoma cells and mesenchyme cells. In contrast, the carcinoma cells seem to be adhesive to the ectoderm cells; desmosomes between the two have been found and also frequent parallel alignment of membranes over long distances. This difference between the interaction of the carcinoma cells with the mesenchyme and the ectoderm may explain why the carcinoma cells can penetrate into the ectoderm but rarely do so into the mesenchyme. The carcinoma cells formed a smooth border with the mesenchyme even in the absence of a basal lamina. These results are discussed in relation to the mechanisms of invasion of epithelial tumours in vivo. In particular, the relative importance of the basal lamina, and cell adhesion within the tumour, in limiting invasiveness are assessed.

Animals↗