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Mark Thompson

Publications and source records attributed to Mark Thompson.

3 recordsLinked to original sources

Antidepressant prescribing in community cancer care.

GOALS: To describe patterns of antidepressant (ADs) prescribing in community oncology practice. PATIENTS AND METHODS: Data were collected using an electronic medical record on all staged breast, colon, and lung cancer patients in three community-based oncology practices. The data were analyzed retrospectively, using descriptive and bivariate analyses and multivariate logistic regression modeling. There were 850 breast, 299 colon, and 473 lung cancer patients identified in this analysis. MAIN RESULTS: Overall, 19.2% of breast, 11% of colon, and 13.7% of lung cancer patients had been prescribed ADs during the 2-year period. The clinic in which cancer treatment was received predicted AD prescribing. The relationship between AD administration and age proved to be nonlinear; the pattern exhibited an "inverted U" shape. Patients with comorbidities and on pain medications were more likely to be administered ADs. Colon cancer patients on pain medications were five times more likely to be administered ADs than those not on pain medications. CONCLUSIONS: While some predictors of AD prescribing appear to be consistent with other studies, such as being on pain medication, there is still a great amount of variability in prescribing patterns across community practices, age groups, and cancer diagnoses. This study demonstrates that prescriptions of ADs seem to be influenced by parameters other than psychopathology. Given the importance of major depression in oncology care, diagnosis of psychiatric disorders and prescription patterns of psychotropics should be part of the routine monitoring and quality management in oncology patient care.

Adult↗

Identification, cloning and expression of the mouse N-acetylglutamate synthase gene.

In ureotelic animals, N-acetylglutamate (NAG) is an essential allosteric activator of carbamylphosphate synthetase I (CPSI), the first enzyme in the urea cycle. NAG synthase (NAGS; EC 2.3.1.1) catalyses the formation of NAG from glutamate and acetyl-CoA in liver and intestinal mitochondria. This enzyme is supposed to regulate ureagenesis by producing variable amounts of NAG, thus modulating CPSI activity. Moreover, inherited deficiencies in NAGS have been associated with hyperammonaemia, probably due to the loss of CPSI activity. Although the existence of the NAGS protein in mammals has been known for decades, the gene has remained elusive. We identified the mouse (Mus musculus) and human NAGS genes using their similarity to the respective Neurospora crassa gene. NAGS was cloned from a mouse liver cDNA library and was found to encode a 2.3 kb message, highly expressed in liver and small intestine with lower expression levels in kidney, spleen and testis. The deduced amino acid sequence contains a putative mitochondrial targeting signal at the N-terminus. The cDNA sequence complements an argA (NAGS)-deficient Escherichia coli strain, reversing its arginine auxotrophy. His-tagged versions of the pre-protein and two putative mature proteins were each overexpressed in E. coli, and purified to apparent homogeneity by using a nickel-affinity column. The pre-protein and the two putative mature proteins catalysed the NAGS reaction but one of the putative mature enzymes had significantly higher activity than the pre-protein. The addition of l-arginine increased the catalytic activity of the purified recombinant NAGS enzymes by approx. 2-6-fold.

Acetyltransferases↗