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Biomedical subjects

C A Stirling

Publications and source records attributed to C A Stirling.

15 recordsLinked to original sources
PubMed2000

Lipoproteins and their subfractions in psoriatic arthritis: identification of an atherogenic profile with active joint disease.

OBJECTIVES: (a) To characterise the lipid profile in psoriatic arthritis and investigate whether there are similarities to the dyslipoproteinaemia reported in rheumatoid arthritis and other inflammatory forms of joint disease; (b) to investigate whether there is an atherogenic lipid profile in psoriatic arthritis, which may have a bearing on mortality. METHODS: Fasting lipids, lipoproteins, and their subfractions were measured in 50 patients with psoriatic arthritis and their age and sex matched controls. RESULTS: High density lipoprotein cholesterol (HDL cholesterol) and its third subfraction, HDL(3) cholesterol, were significantly reduced and the most dense subfraction of low density lipoprotein (LDL), LDL(3), was significantly increased in the patients with psoriatic arthritis. Twenty patients with active synovitis had significantly lower total cholesterol, LDL cholesterol, and HDL(3) cholesterol than their controls. 25% of the patients with psoriatic arthritis had raised Lp(a) lipoprotein levels (>300 mg/l) compared with 19% of controls, but this was not statistically significant. CONCLUSION: Raised levels of LDL(3) and low levels of HDL cholesterol are associated with coronary artery disease. Such an atherogenic profile in a chronic inflammatory form of arthritis is reported, which may be associated with accelerated mortality.

Adult↗
PubMed1990

Combination of insulin with glipizide increases peripheral glucose disposal in secondary failure type 2 diabetic patients.

Twenty Type 2 diabetic patients, recently converted to insulin because of inadequate control on oral hypoglycaemic agents, were studied. Endogenous insulin reserve was measured by glucagon stimulation, and insulin-mediated peripheral glucose disposal by a hyperglycaemic (11 mmol l-1) clamp, measurements being repeated after 8 weeks of glipizide or placebo therapy in addition to the patients' usual insulin. The study was randomized and double blind. Fasting and stimulated C-peptide levels did not change on glipizide or placebo. Insulin-mediated glucose disposal rose from 2.5 (1.5-8.0) (median (range] to 4.2 (2.3-8.4) mg kg-1 min-1 in the glipizide group (n = 9, p less than 0.01), but did not change in the placebo group. Glycosylated haemoglobin did not change in either group, but median fasting plasma glucose fell from 10.6 (6.1-15.1) to 9.0 (6.4-11.2) mmol l-1 in the glipizide group (p less than 0.02). Fasting insulin rose on glipizide from 10.1 (4.0-23.2) to 13.0 (6.4-33.8) mU l-1 (p less than 0.02). Insulin dosage fell in the glipizide group from 36 to 26 U day-1, as 4 patients experienced hypoglycaemic symptoms. HDL-Cholesterol fell in all patients on glipizide, from 0.94 (0.79-2.13) to 0.79 (0.62-1.95) mmol l-1 (p less than 0.01). Combination of insulin with the sulphonylurea glipizide in secondary failure Type 2 diabetic patients leads to increased insulin-mediated peripheral glucose disposal. Glipizide may have an adverse effect on HDL-cholesterol, which is unrelated to change in diabetic control.

Aged↗
PubMed1982

Numbers and sizes of nerve fibres in mouse spinal roots.

The numbers of myelinated and non-myelinated nerve fibres in the spinal roots of one strain of mouse have been counted from electron micrographs and the accuracy of counting procedures assessed. Non-myelinated nerve fibres are present in the ventral roots at all levels though the largest number are found inthe thoracic and L1, L5, L6 and S1 ventral roots. The number is very small in L2, L3, and L4 ventral roots which are those supplying the hind limb. Fibre diameter histograms were obtained from measurements of cross sectional area for myelinated and non-myelinated fibres in L1 and L4 ventral roots. The relationship of myelin thickness to axon diameter shows that to a near approximation the myelin thickness is 1/5 to 1/4 the axon diameter. A measure of circularity was calculated, the ratio of the measured cross-sectional area to the area calculated from the measured perimeter assuming the fibre to be circular, and plotted against the axon perimeter fo L1 and L4 ventral root myelinated fibres, This showed a tendency for larger fibres to be less circular than smaller fibres.

Animals↗
PubMed1978

A simple method for maintaining relative positions of separate tissue elements during processing for electron microscopy.

Molten (328 K) 20% gelatin is used as a 'glue' to hold together separate tissue elements or tissue elements that may be separated when cutting small blocks of tissue for plastic embedding. Standard aldehyde and osmium fixation, dehydration and epoxy embedding are compatible with this as is semi-thin sectioning for light microscopy or thin sectioning for electron microscopy.

Animals↗
PubMed1975

Abnormalities in Schwann cell sheaths in spinal nerve roots of dystrophic mice.

Dorsal and ventral spinal roots at cervical, thoracic, lumbar and sacral levels in dystrophic, dy/dy, mice of both 129/ReJ and C57Bl/6J phenotypes showed a complete lack of Schwann cell sheaths of any sort around the majority of their nerve fibres. This condition, termed amyelination, is more extensive (up to 1-5 cm in length) in the longer lumbar and sacral roots than in the shorter roots or in the proximal regions of the sciatic nerve which are also affected to some extent. Amyelination does not appear to be a consequence of myelin or Schwann cell degeneration, as debris is uncommon. Heterozygous carriers are not affected in any obvious way. Myelinated fibres, with Schwann cells of peripheral origin, occur immediately adjacent to the spinal cord in both dorsal and ventral roots, while in dorsal roots unmyelinated fibres also occur, as in normal animals. Amyelinated fibres begin to appear a few internodal lengths away from the cord and are present until near, or within, the dorsal root ganglion, where they become myelinated again. The portion of an axon which has no myelin begins at a normal appearing paranodal region (termed a half node of Ranvier) at the end of a myelin internode. Resumption of myelination likewise begins at a half node. A few myelinated axons may be seen in any given cross section of a root, but as a rule a given myelinated fibre does not remain myelinated throughout the whole length of the root. It is suggested that the nerve lesions develop where the nerves are lengthening rapidly as the animal grows and changes its shape. How these nerve changes release to those in muscle is conjectural.

Animals↗
PubMedDate not supplied

Electrophysiological observations on the spinal cord of the normal and dystrophic mouse.

A method of carrying out electrophysiological experiments on the mouse spinal cord is described. The conduction velocity in the spinal dorsal roots (DR) of the normal mouse was in the range 10-100 m sec-1 and in the ventral roots (VR) 50-70 m sec-1. In the dystrophic mutant (129 ReJ dy/dy) the conduction velocity for both roots was usually in the range 0.1-2.0 m sec-1. Reflexes from DR to VR were recorded in both mutant and wild type animals and it was concluded that the delays in the mutant reflex were probably due to the slower conduction velocity in the roots. Postsynaptic inhibition and presynaptic inhibition were demonstrated and records were made from Renshaw cells and intracellularly from motoneurones. Delayed activity in spinal reflex paths, probably of supraspinal origin, was more pronounced in the dystrophic mutant. It is concluded that if the dystrophic mouse mutant were to be regarded as a model for human disease then similar reflex delays should be demonstrated in human subjects with muscular dystrophy.

Afferent Pathways↗