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Biomedical subjects

S Cunnane

Publications and source records attributed to S Cunnane.

13 recordsLinked to original sources
PubMed2003

The potential role for arachidonic and docosahexaenoic acids in protection against some central nervous system injuries in preterm infants.

The risk of central nervous, visual, and auditory damage increases from 2/1000 live births in the normal birthweight to > 200/1000 as birthweight falls below 1500 g. Such babies are most likely to be born preterm. Advances in infant care have led to increasing numbers of very-low-birthweight, preterm infants surviving to school age with moderate to severe brain damage. Steroids are one of the current treatments, but they cause significant, long-term problems. The evidence reported here suggests an additional approach to protecting the very preterm infant by supporting neurovascular membrane integrity. The complications of preterm, very-low-birthweight babies include bronchopulmonary dysplasia, retinopathy of prematurity, intraventricular hemorrhage, periventricular leukomalacia, and necrotizing enterocolitis, all of which have a vascular component. Arachidonic acid (AA) and DHA are essential, structural, and functional constituents of cell membranes. They are especially required for the growth and function of the brain and vascular systems, which are the primary biofocus of human fetal growth. Molecular dynamics and experimental evidence suggest that DHA could be the ligand for the retinoid X receptor (RXR) in neural tissue. RXR activation is an obligatory step in signaling to the nucleus and in the regulation of gene expression. Very preterm babies are born with minimal fat stores and suboptimal circulating levels of these nutrients. Postnatally, they lose the biomagnification of the proportions of AA and DHA by the placenta for the fetus. No current nutritional management repairs these deficits. The placental biomagnification profile highlights AA rather than DHA. The resultant fetal FA profile closely resembles that of the vascular endothelium and not the brain. Without this nourishment, cell membrane abnormalities would be predicted. We present a scientific rationale for a common pathogenic process in the complications of prematurity.

Animals↗
PubMed1997

Possible role of the choroid plexus in the supply of brain tissue with polyunsaturated fatty acids.

Delta-6 desaturase was measured in rat brain microvessels and choroid plexus by incubation in the presence of radioactive linoleic acid. Under our conditions, in 21-day-old animals, delta-6 desaturase was not detected in brain microvessels. In contrast, it was present in choroid plexus (about 21 pmol/min per mg protein). In comparison, the activity in brain was much lower (about 1 pmol/min per mg protein) and higher in liver (about 55 pmol/min per mg protein). Interestingly, during development the activity in choroid plexus peaked at day 6 after birth and declined slightly thereafter. The pattern of incorporation of linoleic acid radioactivity was not the same in choroid plexus and microvessels. These results show that delta-6 desaturase was not detected in brain microvessels but was present in choroid plexus.

Aging↗
PubMed1992

Emulsion stability in a total nutrient admixture for total parenteral nutrition.

A total parenteral nutrition solution containing lipid was tested up to 28 days at 4 degrees C followed by an additional 2 days at 22 degrees C (room temperature) for stability of the emulsion. The total nutrient admixture (TNA) contained 1000 ml 10% FreAmine, 1000 ml 50% dextrose, 500 ml 10% Soyacal, electrolytes, vitamins and trace elements. Stability was determined by direct observation, light and electron microscopy, Coulter counter, pH, osmolality, and fatty acid profile. Samples were tested when fresh at 0 hours, after 2 days at 22 degrees C, 14 days at 4 degrees followed by 2 days at 22 degrees C, and 28 days at 4 degrees C followed by 1 and 2 days at 22 degrees C. Light microscopy measured particles greater than 2 microns in diameter; 99% of these particles were less than 6 microns, with no increase with time. Electron microscopy found that lipid particle size increased slightly up to 30 days, at which time the mean diameter was 0.36 +/- 0.01 micron. Coulter counter studies found that lipid droplet diameter increased while at 22 degrees C; however, on day 30, 99% of the particles were less than 1.97 microns. Mean pH and osmolality were 6.35 +/- 0.04 and 1880 +/- 14.5 mOsm/kg, respectively, with no change over time. Analysis of fatty acids by gas chromatography showed that fatty acid profiles and amounts of triglyceride, phospholipid and total lipid did not change. Thus, the emulsion in the TNA was stable for 28 days refrigeration, followed by 2 days at room temperature.

Drug Stability↗
PubMed1989

Acrodermatitis enteropathica with normal serum zinc levels: diagnostic value of small bowel biopsy and essential fatty acid determination.

We report a patient with acrodermatitis enteropathica and a normal serum zinc level in whom the diagnosis was confirmed by plasma phospholipid fatty acid and a small bowel biopsy response to oral zinc therapy. Acrodermatitis enteropathica is a rare autosomal recessive condition of zinc deficiency characterised by chronic diarrhoea associated with failure to thrive, periorificial dermatitis and alopecia, susceptibility to infections and behavioural changes. Diagnosis is usually established by reduced serum zinc levels (classical acrodermatitis enteropathica). Paneth cell abnormalities on electron microscope of a small bowel biopsy can be supportive. A few cases with the typical picture of acrodermatitis enteropathica without hypozincaemia (variant acrodermatitis enteropathica) have been described. The diagnosis of variant acrodermatitis enteropathica to date has been based on an entirely empiric, but nonetheless convincing clinical response to oral zinc therapy. Laboratory aids to diagnosis have been lacking.

Acrodermatitis↗
PubMed1978

Regulation of cytoplasmic calcium: interactions between prostaglandins, prostacyclin, thromboxane A2, zinc, copper and taurine.

The regulation of cytoplasmic calcium is a key process in nerve tissue. Using a smooth muscle model we have shown that prostaglandin (PG) E2 probably regulates entry from extracellular fluid, whereas the release from intracellular stores depends on the interplay between thromboxane (TX) A2, PGEI and prostacyclin. Hormones and other agents interact with this system in the following ways: vasopressin, angiotensin and inositol mobilize arachidonic acid from membrane phospholipids and increase synthesis of PGE2 and TXA2, cortisol blocks this action. Prolactin and zinc mobilize dihomo-gamma-linolenic acid and increase synthesis of PGEI. These effects can be blocked by cortisol, lithium and taurine, three agents which on their own have no effect on basal PG production. Epileptogenic agents like penicillin and picrotoxin also stimulate PG synthesis, while diphenylhydantoin is a PG antagonist and diazepam is a TXA2 antagonist. The effects of all these agents occur at concentrations which are physiological in the case of the natural ones, and readily attained in human plasma in the case of the drgus. In view of recent evidence that calcium may be important in demyelination and considering the established role it plays in nerve conduction and synaptic transmission, we suggest that these observations may be of significance in understanding Friedreich's ataxia.

Animals↗