ABSTRACT
Anatomical models have key applications in radiotherapy, notably to help understand the relationship between radiation dose and risk of developing side effects. This review analyses whether age-specific computational phantoms, developed from healthy subjects and paediatric cancer patient data, are adequate to model a paediatric population. The phantoms used in the study were International Commission on Radiological Protection (ICRP), 4D extended cardiac torso (XCAT) and Radiotherapy Paediatric Atlas (RT-PAL), which were also compared to literature data. Organ volume data for 19 organs was collected for all phantoms and literature. ICRP was treated as the reference for comparison, and percentage difference (P.D) for the other phantoms were calculated relative to ICRP. Overall comparisons were made for each age category (1, 5, 10, 15) and each organ. Statistical analysis was performed using Microsoft Excel (version 16.59). The smallest P.D to ICRP was for Literature (-17.4%), closely followed by XCAT (26.6%). The largest was for RT-PAL (88.1%). The rectum had the largest average P.D (1,049.2%) and the large bowel had the smallest (2.0%). The P.D was 122.6% at age 1 but this decreased to 43.5% by age 15. Linear regression analysis showed a correlation between organ volume and age to be the strongest for ICRP (R2 = 0.943) and weakest for XCAT (R2 = 0.676). The phantoms are similar enough to ICRP for potential use in modelling paediatric populations. ICRP and XCAT could be used to model a healthy population, whereas RT-PAL could be used for a population undergoing/after radiotherapy.
ABSTRACT
The aims of the present study were to determine in 14 healthy subjects and 14 duodenal ulcer patients the reproducibility of the acid secretory response to a modified sham-feeding test and the effect on this response of intrajejunal hypertonic glucose instillation, in order to evaluate the possibility of the existence of a defective inhibition of the cephalic phase of gastric acid secretion in duodenal ulcer disease. The reproducibility of the acid secretory response to a modified sham-feeding test was demonstrated in both groups in two consecutive tests. The hypertonic glucose instillation produced a significant inhibition of the acid secretory response to modified sham feeding only in the healthy subjects, suggesting that duodenal ulcer patients may have a defective mechanism of acid inhibition during vagal stimulation by modified sham feeding. Non-significant changes were observed in plasma gastrin and pancreatic glucagon levels.
Subject(s)
Duodenal Ulcer/physiopathology , Gastric Acid/metabolism , Adult , Female , Food, Formulated , Glucose Solution, Hypertonic , Humans , Instillation, Drug , Jejunum/metabolism , Male , Middle AgedABSTRACT
Acid instillation into the duodenum inhibits basal and stimulated gastric secretion. In man vagotomy suppresses this secretory inhibition. It is postulated that such inhibition responds to a dual mechanism: an hormonal one (enterogastrone) and a nervous one (vagus nerve). This study showed that preoperative duodenal acidification of duodenal ulcer patients results in a decrease in basal gastric secretion and in gastrin levels. On the contrary, in patients submitted to vagal denervation--either through truncal division or highly selective vagotomy--duodenal acidification does not inhibit gastric secretion; however, a drop occurs in basal gastrin levels. An intact gastric vagal innervation therefore, seems necessary for the preservation of the sensitivity of the parietal cell to the effect of hormonal inhibitors, it being immaterial whether duodenal innervation is present or not, as that duodenal acidification provokes a significant fall in serum gastrin levels as determined by radioimmunoassay. This hormonal decrease produced by duodenal acidification can be explained by the inhibition of gastrin release from the antrum. Agreement is expressed with the opinion of other authors that highly selective vagotomy does not appear to carry any advantage over truncal section of the vagus nerves from the standpoint of the inhibitory mechanism of gastric secretion from the duodenum.
