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Patrick Moore

Publications and source records attributed to Patrick Moore.

5 recordsLinked to original sources
PubMed2006

Family history of gastric cancer: a correlation between epidemiologic findings and clinical data.

BACKGROUND: The pathogenetic mechanisms behind gastric cancer are still unclear. Its familial aggregation, on the other hand, has been very well documented by many epidemiologists. Nonetheless, only a limited number of studies have analyzed possible correlations between demographic and clinical data. METHODS: Between January 1988 and August 2004, 541 patients underwent gastric resection with a curative intent at our department; demographic information, laboratory data, imaging, operative notes, and pathology reports were available for all patients. During 2004 we conducted a series of structured interviews with the surviving patients or their closest relatives regarding oncological family history, limited to first-degree relatives. RESULTS: Family history could be obtained in 383 patients (70.8%). Gastric cancer was by far the most frequently associated tumor: 21.9% of the overall number of tumors reported in the family histories were gastric cancers. Patients were also subdivided into those having at least one other family member with stomach cancer (71 patients; 18.5%) and those with no relatives affected by gastric cancer (312 patients; 81.5%). No statistically significant differences between the groups were observed regarding the primary tumor location, size, pTNM classification, and ABO or Rh blood types. However, the intestinal histotype was significantly (P = 0.015) more frequently represented in individuals with at least one family member affected by gastric cancer compared with those with no relatives with stomach cancer (71.8% vs 55.1%, respectively). CONCLUSIONS: Stomach cancer has a relevant degree of familial aggregation and in our series of patients, this was even more pronounced for the intestinal histotype.

Adenocarcinoma↗
PubMed2005

Intrabodies targeting the Kaposi sarcoma-associated herpesvirus latency antigen inhibit viral persistence in lymphoma cells.

Kaposi sarcoma-associated herpesvirus (KSHV) latency-associated nuclear antigen-1 (LANA1) is essential for the maintenance and segregation of viral episomes in KSHV latently infected B cells. We report development of intracellular, rabbit-derived antibodies generated by phage display technology, which bind to N-terminal LANA1 epitopes and neutralize the chromosome-binding activity of LANA1. Although these cloned single-chain variable fragments (scFvs) show relatively low binding affinities for the LANA1 viral antigen in in vitro assays, they nonetheless outcompete KSHV-seropositive human sera for LANA1 epitope binding. In heterologous cells, intracellular intrabody expression inhibits LANA1-dependent plasmid maintenance of both an artificial plasmid containing KSHV LANA1 binding sequences and a bacterial artificial chromosome containing the entire KSHV genome. In KSHV naturally infected primary effusion lymphoma cells, intracellular intrabody expression causes a reduction or loss of the typical LANA1 punctate, nuclear pattern. This morphologically apparent LANA1 dispersion correlates to loss of viral episome by molecular analysis. These data suggest a novel approach to antiherpes viral therapy and confirm LANA1 is critical target for neutralization of KSHV viral latency.

Amino Acid Sequence↗
PubMed2004

A role for the malonyl-CoA/long-chain acyl-CoA pathway of lipid signaling in the regulation of insulin secretion in response to both fuel and nonfuel stimuli.

The malonyl-CoA/long-chain acyl-CoA (LC-CoA) model of glucose-induced insulin secretion (GIIS) predicts that malonyl-CoA derived from glucose metabolism inhibits fatty acid oxidation, thereby increasing the availability of LC-CoA for lipid signaling to cellular processes involved in exocytosis. For directly testing the model, INSr3 cell clones overexpressing malonyl-CoA decarboxylase in the cytosol (MCDc) in a tetracycline regulatable manner were generated, and INS(832/13) and rat islets were infected with MCDc-expressing adenoviruses. MCD activity was increased more than fivefold, and the malonyl-CoA content was markedly diminished. This was associated with enhanced fat oxidation at high glucose, a suppression of the glucose-induced increase in cellular free fatty acid (FFA) content, and reduced partitioning at elevated glucose of exogenous palmitate into lipid esterification products. MCDc overexpression, in the presence of exogenous FFAs but not in their absence, reduced GIIS in all beta-cell lines and in rat islets. It also markedly curtailed the stimulation of insulin secretion by other fuel and nonfuel secretagogues. In the absence of MCDc overexpression, the secretory responses to all types of secretagogues were amplified by the provision of exogenous fatty acids. In the presence of exogenous FFAs, the fatty acyl-CoA synthetase inhibitor triacsin C reduced secretion in response to glucose and nonfuel stimuli. The data show the existence of important links between the metabolic coupling factor malonyl-CoA, the partitioning of fatty acids, and the stimulation of insulin secretion to both fuel and nonfuel stimuli.

Acyl Coenzyme A↗
PubMed2002

Predictors of glycaemic control and hypoglycaemia in children and adolescents with type 1 diabetes from NSW and the ACT.

OBJECTIVES: To audit glycaemic control and incidence of severe hypoglycaemia in children and adolescents with type 1 diabetes in New South Wales (NSW) and the Australian Capital Territory (ACT). DESIGN: A multicentre, population-based, cross-sectional study from 1 September to 31 December, 1999. PARTICIPANTS: 1190 children and adolescents aged 1.2-15.8 years with type 1 diabetes, identified from three hospital-based paediatric diabetes units, four private city-based paediatric practices and 18 regional outreach clinics in NSW and the ACT. MAIN OUTCOME MEASURES: HbA(1c) level and incidence of severe hypoglycaemia (defined by unconsciousness or seizures). RESULTS: The response rate was 67% (1190 of a target group of 1765). The median HbA(1c) level was 8.2% (interquartile range, 7.6%-9.1%). Significant predictors of HbA1c level in a multiple regression model were duration (b = 0.05; 95% CI, 0.02-0.07) and insulin dose/kg (b = 0.46; 95% CI, 0.27-0.66). At least one episode of severe hypoglycaemia in the previous three months was reported in 6.7%, and the rate of severe hypoglycaemia was 36/100 patient-years. Significant predictors of hypoglycaemia in a Poisson regression model were younger age (P = 0.03), male sex (P = 0.04), longer diabetes duration (P = 0.02), and > 3 daily insulin injections (P = 0.02), but not HbA(1c) level. Children with diabetes had higher BMI standard deviation scores compared with population standards, and those in the highest quartile of BMI standard deviation score were younger, had shorter diabetes duration and had higher HbA(1c) level. CONCLUSIONS: Many children and adolescents with type 1 diabetes have suboptimal glycaemic control, placing them at high risk of developing microvascular complications. Those with longer diabetes duration are at increased risk of suboptimal glycaemic control and severe hypoglycaemia and should be targeted for interventional strategies.

Adolescent↗