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Biomedical subjects

J D Murray

Publications and source records attributed to J D Murray.

At least 163 records · Page 9Linked to original sources
PubMed1985

A simple model for the spatial spread and control of rabies.

A simple mathematical model for the spatial spread of rabies is presented. It models the dynamics of the front of an epizootic wave. We show how the model can be used to estimate the minimum width (in kilometers) of a break, that is, a region in which a control scheme is employed in order to stop the spatial progression of the rabies wave front. A simple expression is derived for the surviving fox population, after the passage of the epizootic, in terms of measurable parameters of the model.

Animals↗
PubMed1985

Ovarian response to PMSG treatment in ewes immunized against oestradiol-17 beta.

The effects of active immunization against oestradiol-17 beta on the ovarian response to pregnant mare serum gonadotrophin (PMSG) was investigated in Merino ewes. Immunized (79) and control (41) ewes were synchronized with intravaginal sponges, given either 750 or 1500 i.u. PMSG and then mated to rams or inseminated laparoscopically with fresh diluted semen. All control ewes mated naturally exhibited oestrus and 40 out of 41 control ewes ovulated. The ovulation rate was higher in the controls receiving 1500 i.u. PMSG than in those ewes which received 750 i.u. PMSG (10.2 v. 3.3). Immunization against oestradiol-17 beta resulted in antibody titres varying from 100 to more than 100 000 in plasma taken 1-4 days after mating. The ovarian response increased significantly in the lowest titre group (100-1000) in conjunction with stimulation with 1500 i.u. PMSG. In these ewes the ovulation rate increased over controls (16.7 v. 10.2) as did the total ovarian response, which includes follicles greater than 10 mm diameter (22.3 v. 11.1). The total ovarian response was also increased in those ewes given 750 i.u. PMSG which had titres in the 1000-10 000 and 10 000-100 000 range, but this was not accompanied by significant increases in the ovulation rate. In general, the higher titre levels (greater than 1000) were correlated with decreases in the proportion of ewes showing oestrus and ovulating and in the embryo recovery rate. The 1500 i.u. PMSG treatment group with the highest titres (greater than 10 000) also showed a significant drop in the ovulation rate as compared to the 1500 i.u. PMSG controls.

Animals↗
PubMed1985

Cytogenetic analysis of 34 early stage bovine embryos from superovulated Hereford donors.

One hundred and thirty-four bovine embryos were collected from 17 superovulated Hereford cows and processed for metaphase chromosome spreads. Mitotic figures were obtained from 54 embryos (40%), but only 34 embryos (25%) provided analyzable chromosomes spreads. Thirty embryos were 2n = 60, one was a possible 2n/4n mosaic and three were hypodiploid. The hypodiploid cases and the 2n/4n mosaic could be due to technical artifacts.

Animals↗
PubMed1985

Occurrence of haploid and haploid/diploid mosaic embryos in untreated and androstenedione-immune Australian Merino sheep.

Chromosome counts were obtained from 73 out of 177 (41%) early cleavage-stage Merino embryos. A further 13 embryos were classified as probably diploid. Chromosome aberrations were found in 8 (11%) embryos, one of which was aneuploid and the remainder (9.6%) had euploid abnormalities. If the probable diploid embryos are included, the incidence of euploid aberrations falls to 8.1%. Of the abnormal embryos there was one aneuploid with 2N = 55, two haploids, four haploid/diploid mosaics and one zygote with 4 haploid metaphase plates. Two additional zygotes had 4 interphase pronuclei. Four of the euploid abnormalities were attributable to the entry of two or more spermatozoa and therefore polyspermy is the largest single factor leading to chromosomally aberrant embryos in this population of Merino ewes.

Androstenedione↗
PubMed1985

A model for chondrogenic condensations in the developing limb: the role of extracellular matrix and cell tractions.

The hyaluronate component of the extracellular matrix is a powerfully hydrophilic polymer, capable of osmotically swelling and deswelling by a volume factor of 5 or more. At the time of cartilage condensation in the limb bud the chondrocytes start to produce hyaluronidase, an enzyme which degrades hyaluronate. The consequent deswelling brings the chondrocytes closer together - close enough for intercellular cell tractions to become effective and intercellular junctions to form. By analysing the physicochemical situation we show how these processes, principally the coupling of the osmotic deswelling with cellular traction forces, can produce cartilage condensation patterns resembling those in the early limb bud. In distinction from our earlier model for chondrogenic condensations this mechanism does not depend on cell motions other than convective transport by contraction.

Animals↗
PubMed1984

Cell traction models for generating pattern and form in morphogenesis.

During early development migratory mesenchymal cells navigate to distant sites where they aggregate to form a variety of embryonic organ rudiments. We present here a new model for mesenchymal cell morphogenesis based on the mechanical interaction between motile cells and their extracellular environment. The model is based on two properties of motile cells: (a) they are capable of generating large traction forces which can deform the extracellular matrix through which they move, and (b) the deformations they produce in their environment affect the direction of their movements. We derive field equations which describe the motion of cells in an elastic extracellular matrix and show that these equations can generate a variety of spatial patterns, such as the formations of skin organ primordia, especially feather germs, cartilage condensation patterns which presage bone formation in limb development, and melanocyte density patterns which form animal coat patterns.

Animals↗
PubMed1984

Generation of biological pattern and form.

We propose two models for pattern formation in early embryogenesis. The first deals with patterns in motile mesenchymal cells; the second treats patterns in epithelial sheets. In the mesenchymal model, cells exert tractions which deform the extracellular matrix within which they move. This in turn affects their motion. The model field equations are formulated and analysed, and applied to two widely studied phenomena: skin-organ primordia for feather and scale patterns, and the development of cartilage patterns in limb bone formation. The model for epithelial pattern formation consists of viscoelastic field equations with a calcium-controlled contraction trigger. Preliminary analysis is presented which demonstrates the existence of travelling wave solutions.

Animals↗
PubMed1984

Triple chromosome pairing in an aneuploid bull spermatocyte.

A triple synaptonemal complex was observed between three midsized chromosomes in an aneuploid bull spermatocyte. Fifteen other spermatocytes examined from the same animal displayed normal chromosome complements and pairing. This is the second case reported of triple synapsis in a mammal and the first case in an apparently normal individual.

Aneuploidy↗
PubMed1983

Minimum domains for spatial patterns in a class of reaction diffusion equations.

We study a general class of scalar reaction/interacting population diffusion equations in two space dimensions: convective terms, due to wind, are included. We consider boundary conditions which include a measure of the hostility to the species in the exterior of the domain. The main point of the paper is to obtain estimates for the minimum domain size which can sustain spatially heterogeneous structures and indicate the type of patterns which could appear.

Animals↗
PubMed1983

Mechanical aspects of mesenchymal morphogenesis.

Many embryonic cells generate substantial contractile forces as they spread and crawl. These forces mechanically deform each cell's local environment, and the resulting distortions can alter subsequent cell movements by convection and the mechanisms of contact guidance and haptotaxis. Here we develop a model for the cumulative effects of these cell-generated forces and show how they can lead to the formation of regular large-scale patterns in cell populations. This model leads to several predictions concerning the effects of cellular and matrix properties on the resulting patterns. We apply the model to two widely studied morphogenetic processes: (a) patterns of skin-organ primordia, especially feather germ formation, and (b) the condensation of cartilagenous skeletal rudiments in the developing vertebrate limb.

Animals↗
PubMed1982

Altered cell cycle progression and aberrant mitosis in adenovirus-infected rodent cells.

Actively growing mouse or rat embryo cells suffered structural chromosome damage, mitotic anomalies, and polyploidy after infection by human adenovirus type 5. Chromosome damage required expression of one or more early viral genes and showed regular periodicity in its frequency. The growth cycle time of some of the infected cells was reduced by about 5 hours due to a decrease in G1, and the interval between successive waves of chromosome damage corresponded to this reduced cycle time. After infection there was a decrease in cells with G1 DNA content and an increase in cells with G2 diploid, aneuploid, and polyploid DNA contents. We suggest these effects are due to the expression in semipermissive cells fo early viral gene(s), whose function in productive infection in vivo is to alter cell cycle controls in order to maximize the number of cells able to replicate viral DNA and the time such cells spend in DNA replication.

Adenoviridae Infections↗
PubMed1982

Adenovirus-induced alterations of the cell growth cycle: effects of mutations in early regions E2A and E2B.

Mutants ts125 (E2A) and ts36 (E2B) of adenovirus type 5 induced alterations to cell cycle progression at the nonpermissive temperature which were detectable by flow cytometry. Thus neither E2A, nor gene N in E2B, is required for these effects. Whereas the wild-type virus induced cells with aneuploid (between 4n and 8n) DNA contents, as did ts125 at the permissive temperature, ts125 induced peaks of cells with 8n, 16n, and 32n DNA contents at the nonpermissive temperature. This was probably due to the failure of regulation of E1A by E2.

Adenoviruses, Human↗
PubMed1982

A model of L(+)-lactate metabolism in normal man.

Mathematical models were used to study the elimination of L(+)-lactate during and after an intravenous load of unlabelled sodium L(+)-lactate in 20 normal postprandial subjects. Clearance of L(+)-lactate from blood was 17.9 +/- 1.1 ml (kg BW)-1 min-1 and the endogenous production rate of L(+)-lactate at rest was 1.38 +/- 0.16 mol (70 kg BW)-1 24 h-1. Clearance and production were unchanged after a 36-hour fast in 4 subjects. Renal excretion of L(+)-lactate accounted for less than 1.2% of the infused load. Clearance of L(+)-lactate was closely related to the pre-infusion concentrations of ketone bodies and alanine.

Adult↗
PubMed1982

Utilization of L(+) lactate in patients with liver disease.

Clearance of intravenously infused sodium L(+) lactate was slower in 37 patients with liver disease (14.5 +/- 0.9 ml (kg BW)-1min-1) than in 20 normal subjects (17.9 +/- 1.1 ml (kg BW)-1min-1). This difference is statistically significant (2p less than 0.0125). Impairment of L(+) lactate utilization was not related to the aetiology of the liver disease. Both increased production and decreased utilization of L(+) lactate were found in patients with secondary malignancy of the liver. Penetration of L(+) lactate into ascitic fluid was variable and estimates of L(+) lactate utilization may be unreliable if ascites is present.

Adult↗