Objective. To evaluate the utility of magnetic resonance imaging (MRI) and P-31 magnetic resonance spectroscopy (MRS) in the longitudinal management of patients with dermatomyositis (DM).Methods. The study group consisted of 11 patients, including 3 children, all of whom had a clinical diagnosis of DM. A control group of 8 subjects was studied simultaneously. MRI included images as well as calculations of T1 and T2 relaxation times. The P-31 MRS protocol evaluated metabolic status (i.e., inorganic phosphate/phosphocreatine ratios and phosphocreatine and ATP levels) during rest, exercise, and recovery.Results. T2-weighted images of the thigh muscles showed inflammation even when serum creatine phosphokinase levels were in the normal range. Metabolic abnormalities, which were accentuated with exercise,
Neuropeptides and their corresponding G protein-coupled receptors (GPCRs) are increasingly implicated in the autocrine/paracrine stimulation of growth of human cancers. We report that neurotensin induced rapid Ca2+ mobilization from intracellular stores followed by Ca2+ influx in five human ductal pancreatic cancer cell lines: HPAF-II, Capan-1, Capan-2, PANC-1, and MIA PaCa-2. In addition, most cell lines exhibited Ca2+ responses to multiple neuropeptides including bombesin, bradykinin, cholecystokinin, and vasopressin and to bioactive lipids, including lysophosphatidic acid (LPA), that also act via GPCRs. The well-differentiated line HPAF-II responded to at least seven independent GPCR agonists. The concentrations of neurotensin required to induce half-maximal effects (EC50) in HPAF-II and PANC-1 cells were 5 and 8nM, respectively. Digital fluorescence image analysis to measure Ca2+ responses in single cells revealed that 90% or more of HPAF-II and PANC-1 cells responded to 10nM neurotensin. Addition of neurotensin to PANC-1 cells also induced rapid and dose-dependent extracellular-regulated protein kinase (ERK-1 and ERK-2) activation and subsequently, stimulated DNA synthesis. The signaling complexity of GPCRs uncovered by these studies reveals a new aspect in the biology of human pancreatic cancer and could offer the basis for new approaches to the treatment of this disease.
JDM patients can be monitored with noninvasive P-31 MRS without sedation. Biochemical defects in energy metabolism are concordant with the weakness and fatigue reported by JDM patients. Quantitative MRS data are useful for evaluating patients and optimizing drug treatment regimens.
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