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Biomedical subjects

J A Dickson

Publications and source records attributed to J A Dickson.

At least 37 records · Page 2Linked to original sources

Anorectal malformations with sacral bony abnormalities.

A range of anorectal malformations with sacral bony abnormalities was found in members from three generations of two kindreds. The anorectal anomaly was low in all but one of the patients. Partial sacral agenesis was the main bony defect in one family, and meningomyelocele and spina bifida occulta were noted in the second. The inheritance pattern in these kinships is autosomal dominant. This may be a variant of caudal regression syndrome, which seems to be aetiologically heterogeneous.

Abnormalities, Multiple↗

What happens to the pylorus after pyloromyotomy?

The rate of return to normal of the pylorus muscle in infantile hypertrophic pyloric stenosis was measured by ultrasound, using a simple pyloric volume calculation and a pyloric muscle index. The muscle hypertrophy took from two to 12 weeks to resolve.

Follow-Up Studies↗

Intestinal disease in cystic fibrosis.

Three children with cystic fibrosis developed steatorrhoea unresponsive to changes in pancreatic supplements. The final diagnoses were chronic giardiasis, stagnant loop syndrome, and Crohn's disease. Refractory intestinal symptoms in cystic fibrosis merit further investigation.

Adolescent↗

Acute abdominal pain in children.

This preliminary communication describes the initial results of a further special study investigating the disease spectrum and clinical presentation in a total of 1080 children admitted to hospital with acute abdominal pain (677 from the Children's Hospital, Sheffield, England, and the remaining 403 from hospitals in Paris, Oslo, Copenhagen, and Deventer). The disease spectrum in children differs radically from that in adults, well over 90% of cases being due to either acute appendicitis or non-specific abdominal pain (NSAP). The clinical presentation of both appendicitis and NSAP was found to differ from that in older age groups. These findings imply clearly that the use of the existing OMGE database for computer-aided diagnosis--using data drawn from cases of all ages--may not be optimal in children. A fresh database (using only children's data) was therefore created and tested. Its sensitivity for appendicitis was equivalent to that of inexperienced clinicians (79.6% versus 77.3%). The computer's specificity (over 70%) was higher than that of clinicians (52.7%). The findings also re-emphasise the value of disciplined data collection, and the implications for teaching are discussed.

Abdomen, Acute↗

Infantile hypertrophic pyloric stenosis--diagnosis from the pyloric muscle index.

Measurements of pyloric length, diameter and muscle thickness were made from ultrasound images of 39 babies, 21 of whom were subsequently found at operation to have infantile hypertrophic pyloric stenosis. From these measurements, the volume of pyloric muscle in cm3 was estimated for each case and divided by the body weight in kilograms. The resulting pyloric muscle index proved to be a much more reliable guide to the diagnosis of pyloric stenosis than any of the individual measurements or the volume estimation alone.

Humans↗

Ruptured ovarian cyst as a cause of ascites in a newborn infant.

Symptomatic ovarian cysts in newborn are rare. In a recent series of cases of congenital ascites ( Griscom et al 1977) only one case out of 27 was caused by an ovarian cyst. We describe a case in which congenital ascites was caused by a ruptured corpus luteum ovarian cyst.

Ascites↗

Abdominal nocardiosis in a Sudanese girl.

A Sudanese girl became desperately ill with liver and kidney abscesses due to Nocardia asteroides. She did not have pulmonary or cutaneous infection. She recovered after surgical drainage of the abscesses and prolonged treatment with intravenous amikacin and high dosage cotrimoxazole and sulphadimidine. After recovery normal neutrophil function, cell-mediated and humoral immunity were demonstrated.

Abscess↗

Colonic neuronal dysplasia.

A child with colonic neuronal dysplasia is reported in whom the whole length of the colon was involved. Multiple colonoscopic mucosal biopsies with acetylcholinesterase staining provided a useful means of assessing the extent of the lesion. Colectomy has, so far, been resisted in view of the relatively mild symptoms in a child who is otherwise thriving. The neonatal necrotising enterocolitis in this case is probably related pathogenetically to that sometimes seen in Hirschsprung's disease. Greater awareness of this condition and the more frequent use of acetylcholinesterase staining of rectal biopsy tissue will probably uncover more cases.

Acetylcholinesterase↗

Hyperthermia: the immune response and tumor metastasis.

Evidence is circumstantial that in animals and, to some extent, in man, an antitumor immune response may be generated after curative hyperthermia that leads to disappearance of metastases (abscopal response) and the acquisition of host immunity. In rodents, tumor regression after heating does not occur in immunosuppressed hosts, and the tumor cure rate is significantly reduced by inhibition of macrophage activity with silica; cured immune rats succumb to tumor inoculation when immunosuppressed. Quantitative data for cellular and humoral immunocompetence in these situations exist for only a few tumor types, and the bulk of evidence indicates that host response following tumor heating is nonspecific in type, with a major macrophage component. Little is distinctive about the regression of heated tumors, i.e., an abscopal response can follow treatment of tumors by excision or hypothermia. In man, an immune response is seldom evoked by the heating of the common solid tumors. Whole-body heating in animals can cause immunosuppression, probably from a direct damaging effect on lymphoid tissue, and enhanced metastatic spread may follow in the tumor-bearing host, but this has not been proved in man. The differences in response of tumors to heat in animals and man may be due to variations in tumor immunogenicity and host tolerance to heat.

Animals↗

Influence of tumour volume and cell kinetics on the response of the solid Yoshida sarcoma to hyperthermia (42 degrees C).

The cytokinetic response of the solid Yoshida sarcoma to hyperthermia was examined at two tumour volumes, 1.0-1.5 ml and 3.0-3.5 ml. The tumour, growing on the feet of rats, was heated at 42 degrees C for 1 h by water-bath immersion. The larger tumour grew more slowly than the smaller one (doubling time 144 h vs 36 h) due to a halving in growth fraction from 67.8 to 39.6% and an increase in cell-loss factor from 59 to 75.9%. Cell cycle and phase times were similar at both volumes. The effect of heat on the population kinetics at both volumes was similar but complex, and involved delayed cell death after up to 10 mitoses. Initial cell killing and blockade of cell-cycle progression (0-24 h) was followed by recovery of proliferation due to recruitment of cells from the non-proliferative compartment, cell cycle and phase times remaining unaltered. From 48 h, the proliferation rate declined progressively, and tumours were completely necrotic 7-8 days after heat. The damaging effects of heat were at least as severe in the large tumours with a low labelling index and small growth fraction as in the smaller tumours with a much larger compartment of proliferating cells and shorter doubling time. The results imply that there may be no simple relationship between proliferative status and thermosensitivity of a tumour, and illustrate the difficulty in predicting tumour response to heat on the basis of cytokinetic studies.

Animals↗

Effect of hyperglycemia on blood flow, pH, and response to hyperthermia (42 degrees) of the Yoshida sarcoma in the rat.

Hyperglycemia (blood glucose, > 20 mmol/liter) caused a 90 to 100% inhibition of blood flow in the solid Yoshida sarcoma of rat feet, as measured by the fractional distribution of 86Rb and 133Xe clearance. Blood flow through the normal gastrocnemius muscle was increased by 50%, while liver blood flow remained unaltered. Hyperglycemia abrogated the temperature differential (approximately 1 degree) between the heating bath and the tumor, promoting more uniform tumor heating. During the period of reduced blood flow, the pH of the tumor extracellular fluid, measured by miniature glass electrode, declined from 7.19 to 6.63 due to decreased efflux of lactate from the tumor. Tumor intracellular pH, measured by partitioning of dimethyloxazolidinedione across the cell membrane, increased from 7.21 to 7.36. At a very high blood glucose concentration (50 mmol/liter), the tumor was isolated from the host, with almost total blockade of water, chloride, glucose, lactate, and dimethyloxazolidinedione exchange between the tumor and the blood. Hyperglycemia therefore represents a convenient means of isolating the Yoshida sarcoma from the host blood supply to enable more selective treatment with hyperthermia and possibly other modalities.

Animals↗