PubMed Health⌕ Search

Biomedical subjects

P Fullerton

Publications and source records attributed to P Fullerton.

7 recordsLinked to original sources
PubMed2000

Growth hormone use in transitioning patients--clinician and payer concerns.

Determining which patients with childhood-onset growth hormone (GH) deficiency will require continuing GH therapy into and/or throughout adulthood raises clinical and economic issues, such as retesting, appropriate dosing, and the risks and benefits of uninterrupted GH treatment versus the discontinuation of therapy. In his review of the evaluation and management of patients transitioning from GH therapy in childhood to GH therapy in adulthood, Dr. Stephen LaFranchi focuses on the odds of having ongoing GH deficiency, the changes that occur when therapy is discontinued, appropriate follow up of patients who discontinue treatment, and issues regarding the reinitiation of therapy. Dr. Margaret H. MacGillivray addresses appropriate monitoring and follow up of patients in transition, as well as their classification by etiology and severity of GH deficiency. Dr. Pete Fullerton explores new issues regarding GH deficiency treatment from a managed care perspective.

Adolescent↗
PubMed1986

Low birthweight and mortality in Australian Aboriginal babies at the Royal Darwin Hospital: a 15 year study.

A retrospective analysis was made of all births at the Royal Darwin Hospital from 1 January 1969 to 31 December 1983. The births were divided into weight categories and racial groups (Aboriginal and non-Aboriginal). The study showed that there was a 23.2% incidence of low birthweight (LBW) babies (less than 2500 g) in Aboriginals compared with an incidence of 6.4% in non-Aboriginals. It was found that Aboriginals had a better chance of surviving the neonatal periods than non-Aboriginals of the same birthweight for all birthweights up to 2500 g. It is suggested that this occurred because most LBW Aboriginals were more mature than their birthweight would have suggested. The perinatal and neonatal mortality, however, remains high in the Aboriginal babies and this can also be attributed to the high incidence of LBW babies in this group, and perhaps to the limited use of antenatal care by the Aboriginal mothers.

Australia↗
PubMed1980

Wound botulism.

It is well recognized that food contamination can result in botulism either from ingestion of performed toxin, in classical botulism, or through absorption of toxin from bacteria within the gut, in infant botulism. Botulism due to contamination of wounds with Clostridium botulinum is not commonly recognized. We report a case of wound botulism occurring in an eight-year-old boy, characterized by early ptosis, dysphagia and dysarthria and then followed by progressive generalized paralysis and fixed dilated pupils, but with intact sensorium. Management consisted of early wound debridement and prolonged intensive respiratory and nutritional support. Recovery was complete.

Botulism↗
PubMed1980

Protein synthesis and the presence of absence of a measurable G1 in cultured Chinese hamster cells.

V79-8 cells lack a measurable G1 interval under normal growth conditions. We found that partial inhibition of protein synthesis using low levels of cycloheximide (0.05 mu/ml) could induce a measurable G1 in these cells without any significant effects on S, G2, or M. In view of these findings, recessive mutants selected from the V79-8 cell line, which each express G1, were analyzed for their rates of protein synthesis and degradation/loss. Three of the four mutants showed a decreased rate of protein synthesis sufficient to account for their G1 lengths. A fourth mutant, however, showed parental rates of both protein synthesis and degradation/loss. These results suggest not only that a G1 interval can be expressed as a result of a decreased rate of protein synthesis, but that other alterations (mutations) other than those simply affecting overall protein synthesis can result in the expression of a measureable G1 interval.

Animals↗
PubMed1975

Hemophagocytic reticulosis. A case report with investigations of immune and white cell function.

A 5-month-old child with hemophagocytic reticulosis is described. Investigations revealed a grossly defective PHA response of the patient's lymphocytes which improved with chemotherapy. Defective glucose oxidation by phagocytosing cells and low IgA levels were demonstrated at diagnosis and have persisted despite chemotherapy. HL-A typing and chromosome studies did not reveal maternal lymphocytes in the child's circulation. The patient was treated with vinblastine and prednisolone and remains well after 11 months of treatment.

Antibody Formation↗