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Biomedical subjects

S J Parry

Publications and source records attributed to S J Parry.

7 recordsLinked to original sources
PubMed1995

The determination of 129I in milk and vegetation using neutron activation analysis.

A new method has been developed to measure 129I in the environment with detection limits below 10 mBq/kg of vegetation and 10 mBq/l of cows' milk. The method is based on extraction of 129I from the milk or vegetation sample, onto an ion exchange resin. An inactive carrier of 127I is added to the sample before separation, to monitor losses throughout the entire procedure. The ion exchange resin is irradiated for 7.5 h in a neutron flux of 10(16) n m-2 s-1 to induce the 129I(n, gamma) 130I reaction with thermal neutrons. The 127I carrier undergoes a (n,2n) reaction with fast neutrons to produce 126I. Iodine is extracted from the ion exchange resin after irradiation with an elution scheme which removes contamination from the radionuclide 82Br, the main interference in the analysis. Finally iodine is precipitated as AgI for gamma ray analysis. The sample is counted for 3 h on a Ge semiconductor detector to measure the radionuclide 130I, which has a half life of 12.4 h and 126I, which has a half life of 13.0 days. The measured 130I activity is compared to a known standard to deduce the amount of 129I in the sample, and the concentrations are corrected for losses during processing using the measured activity of 126I. The detection limits for 129I by this method are below 10 mBq/l for milk samples and 10 mBq/kg for vegetation. In addition to routine monitoring of milk and grass samples the method has been used to measure 129I deposition on grass and soils in a field near the Sellafield plant. Results of these analyses, along with measurements of 129I in air and rainfall using the same methodology, have been used to determine deposition velocity and retention coefficients of 129I to grass.

Animal Feed↗
PubMed1994

Redundant parasympathetic and sympathoadrenal mediation of increased glucagon secretion during insulin-induced hypoglycemia in conscious rats.

Both the parasympathetic and sympathoadrenal inputs to the pancreas can stimulate glucagon release and are activated during hypoglycemia. However, blockade of only one branch of the autonomic nervous system may not reduce hypoglycemia-induced glucagon secretion, because the unblocked neural input is sufficient to mediate the glucagon response, ie, the neural inputs are redundant. Therefore, to determine if parasympathetic and sympathoadrenal activation redundantly mediate increased glucagon secretion during hypoglycemia, insulin was administered to conscious rats pretreated with a muscarinic antagonist (methylatropine, n = 7), combined alpha- and beta-adrenergic receptor blockade (tolazoline + propranolol, n = 5) or adrenergic blockade + methylatropine (n = 7). Insulin administration produced similar hypoglycemia in control and antagonist-treated rats (25 to 32 mg/dL). In control rats (n = 9), plasma immunoreactive glucagon (IRG) increased from a baseline level of 125 +/- 11 to 1,102 +/- 102 pg/mL during hypoglycemia (delta IRG = +977 +/- 98 pg/mL, P < .0005). The plasma IRG response was not significantly altered either by methylatropine (delta IRG = +677 +/- 141 pg/mL) or by adrenergic blockade (delta IRG = +1,374 +/- 314 pg/mL). However, the IRG response to hypoglycemia was reduced to 25% of the control value by the combination of adrenergic blockade + methylatropine (delta IRG = +250 +/- 83 pg/mL, P < .01 v control rats). These results suggest that the plasma glucagon response to hypoglycemia in conscious rats is predominantly the result of autonomic neural activation, and is redundantly mediated by the parasympathetic and sympathoadrenal divisions of the autonomic nervous system.

Adrenal Glands↗
PubMed1994

Evaluation of 153Sm-diethylenetriaminepentaacetic acid for radiolabelling of pharmaceutical dosage forms by neutron activation.

153Sm-DTPA provides a suitable alternative to 99mTc-DTPA and 111In-DTPA as a water soluble tracer for the evaluation of pharmaceutical preparations. The chelate was handled biologically in a similar way to 99mTc-DTPA and 111In-DTPA. The chelate can be incorporated into the formulation as a non-radioactive excipient and the intact dosage form can then be neutron activated to produce 153Sm.

Administration, Inhalation↗
PubMed1993

Environmental and personnel monitoring for uranium by delayed neutron counting.

At the Imperial College Reactor Centre we have developed a fully automated, large sample, high sensitivity delayed neutron counting system for routine analysis of environmental samples and personnel monitoring. Two-hundred fifty samples with a maximum volume of 30 ml can be analysed each working day. The detection limits (3 sigma) for uranium of natural isotopic abundance in our routine samples are typically 1 microgram/kg (0.05 Bq/kg) for dry samples and 1 microgram/l (0.05 Bq/l) for aqueous samples. Daily analysis of BNFL uranium standards, 'in house' uranium standards and weekly analysis of IAEA Soil-7 reference material are used to ensure constant system sensitivity and accuracy.

Humans↗
PubMed1992

The characterization of radioimmunoassay for rat pancreatic polypeptide in serum.

A radioimmunoassay for the measurement of rat pancreatic polypeptide (RPP) in serum or plasma has been developed and characterized using a new guinea-pig anti-rat-PP antibody. The assay provides a high degree of sensitivity and lacks cross-reactivity (CR less than 0.01%) to neuropeptide Y and peptide YY. It also does not interact with PPs of other species or peptide hormones namely, amylin, glucagon, human insulin, human-PP, human-proinsulin, rat C-peptide and rat insulin. The assay employs synthetic rat PP as standards from concentrations of 21-2100 pg/ml (i.e., 5-500 pM) and produces a sensitivity limit of 19 pg/ml (4.5 pM) PP at +/- 3 S.D. The intra- and interassay % coefficient of variations are 6.4% and 5.9%, respectively. The % recovery of RPP added to rat serum samples ranges from 98% to 103%. Assay of serum volumes ranging from 25 microliters to 100 microliters does not significantly alter the expected RPP level. The migration patterns of rat serum PP and that of a synthetic RPP are identical by Sephadex G-50 chromatographic analysis. The mean values of fasting and a 2 h post-feeding plasma RPP levels in normal rats are 40 +/- 2 and 80 +/- 10 pg/ml (9.5 pM and 19.0 pM), respectively. Rat-PP release during insulin induced hypoglycemia in conscious rats rises from 38 +/- 5 pg/ml to 261 +/- 34 pg/ml (9.0 to 62.1 pM, P less than 0.005) by 30 min. Additionally, the antibody used in this study cross-reacts well with mouse-PP as determined by linear serum dilution curves, thus making it useful in the measurement of murine-PP. In conclusion, we have developed and validated a sensitive and specific rat-PP assay. This assay provides a new tool for the reliable measurement of PP in physiologic studies using rat and mouse animal models.

Animals↗
PubMed1992

Autonomic nervous system mediation of the pancreatic polypeptide response to insulin-induced hypoglycemia in conscious rats.

To investigate the neural regulation of pancreatic polypeptide (PP) secretion during hypoglycemia in the rat, insulin was administered to chronically cannulated rats, and plasma PP responses were compared between saline-treated animals and animals pretreated with a ganglionic blocking agent (hexamethonium), a muscarinic antagonist (atropine), combined alpha- and beta-adrenergic receptor blockade (propranolol + tolazoline), or combined adrenergic blockade + atropine. PP was measured using a new RIA which selectively detects PP in rat plasma. In control rats (n = 10), plasma PP increased from a baseline level of 30 +/- 3 pg/ml to 271 +/- 41 pg/ml during hypoglycemia (plasma glucose = 29 +/- 2 mg/dl) (delta PP = +241 +/- 42 pg/ml, P less than 0.0005), demonstrating that in rats, as in other species, insulin-induced hypoglycemia is a potent stimulus for PP release. PP only increased by 31 +/- 10 pg/ml during similar hypoglycemia in 7 hexamethonium-treated rats (P less than 0.01 vs. control animals). Thus, at least 90% of the PP response to hypoglycemia is neurally mediated. The plasma PP response to hypoglycemia was +85 +/- 24 pg/ml in atropine-treated rats (P 0.01 vs. control rats), suggesting that approximately 65% of the PP response is mediated via muscarinic acetylcholine receptors on the islet F cell. The PP response to hypoglycemia in rats with combined adrenergic blockade (delta = +168 +/- 32 pg/ml) was slightly, but not significantly smaller than that in control rats. The combination of combined blockade + atropine resulted in a PP response (delta = +26 +/- 7 pg/ml) to hypoglycemia that was similar to that in hexamethonium-treated rats (P less than 0.01 vs. control rats). These results suggest: 1) The PP response to hypoglycemia is predominantly the result of muscarinic, cholinergic activation. 2) There is a minor adrenergic contribution to the response. 3) The plasma PP response may be useful as an index of autonomic neural input to the islet during hypoglycemia.

Animals↗