Echovirus 30 meningitis epidemic followed by an outbreak-specific RT-qPCR.

BACKGROUND: An outbreak of enteroviral aseptic meningitis emerged in Southwestern Finland in August 2009. The same enterovirus reappeared with increasing incidence of meningitis in other parts of Finland in 2010. OBJECTIVES: To identify the incidence and molecular epidemiology of enteroviral meningitis outbreak. STUDY DESIGN: The causative agent was identified as echovirus 30 (E-30) by sequencing partial viral protein 1 capsid genome, and a virus type-specific RT-qPCR was set up for sensitive detection of the virus in cerebrospinal fluid specimens. Enterovirus positive CSF specimens were subjected to the E-30-specific assay to investigate this unusual occurrence of aseptic meningitis and facilitate case confirmation during the outbreaks between August 2009 and September 2010. RESULTS: E-30 was detected in 106 (72%) enterovirus positive cerebrospinal fluid specimens. All the meningitis cases in 2009 and most of them in 2010 were among adolescents and several were members of sport teams. CONCLUSIONS: Between August 2009 and September 2010, E-30 caused an extensive outbreak with two peaks in Finland. Type-specific RT-PCR allowed rapid diagnostic follow-up of the epidemic.

6-[18F]fluoro-L-DOPA uptake in the rat pancreas is dependent on the tracer metabolism.

PURPOSE: 6-[(18)F]fluoro-L-3,4-dihydroxyphenyl alanine ([(18)F]FDOPA) positron emission tomography (PET) is a diagnostic tool which can detect malignancies of the pancreas. We aimed to study whether the manipulation of the [(18)F]FDOPA metabolic pathway would change the (18)F-behavior to provide a biochemical foundation for PET imaging of rat pancreas with [(18)F]FDOPA. PROCEDURES: Inhibitors of aromatic amino acid decarboxylase, catechol-O-methyltransferase, monoamine oxidases A and B, or their combinations on [(18)F]FDOPA uptake, metabolism, and the regional distribution in the rat pancreas was evaluated using in vivo PET/computed tomography imaging, chromatographic metabolite analyses, and autoradiography. RESULTS: Enzyme inhibition generally increased the uptake of [(18)F]FDOPA derived (18)F-radioactivity in rat pancreas. Dependent on which enzymatic pathway is blocked (or a combination of pathways), different radiolabeled metabolites in pancreas are responsible for this increase in uptake. CONCLUSIONS: Altering the metabolism of [(18)F]FDOPA by using various enzymatic inhibitors increased the radioactivity uptake and changed the radiometabolic profile in the pancreas allowing better discrimination between pancreas and surrounding tissues of rat. However, these manipulations did not separate islets from the exocrine pancreas. Elucidating the metabolic behavior of [(18)F]FDOPA provides a biochemical foundation of PET imaging of the rat pancreas.

Pancreatic glucose uptake in vivo in men with newly diagnosed type 1 diabetes.

CONTEXT: Due to the restricted accessibility of pancreatic tissue in living man, direct analysis of the events preceding development of autoimmune changes in the pancreas has been problematic. In vivo imaging of insulitis might markedly increase understanding of the events and timing of the events that are necessary for the progression toward overt type 1 diabetes. DESIGN: To evaluate possibilities to visualize insulitis in man in vivo with positron emission tomography, we studied 12 male patients (age 26 +/- 7 yr) with newly diagnosed type 1 diabetes (duration range 0-7 months) and nine age- and sex-matched healthy controls after an overnight fast using 2-[(18)F]fluoro-2-deoxy-D-glucose and [(11)C]methionine. For definition of the regions of interest, pancreas was localized with magnetic resonance imaging or computed tomography-positron emission tomography. RESULTS: Glucose uptake to the pancreas was markedly higher in the patients with type 1 diabetes than in the healthy controls (22.9 +/- 6.4 vs. 17.8 +/- 6.0 micromol/kg.min, P = 0.039). Glucose uptake to the pancreas of the patients was inversely associated with the duration of diabetes (r = -0.58; P = 0.024), so that in patients with newly diagnosed type 1 diabetes, glucose uptake was higher than in the healthy controls or patients with long duration of diabetes. Methionine uptake to the pancreas of the patients was similar as in the controls (3.7 +/- 1.9 vs. 4.6 +/- 2.4 micromol/kg.min, P = 0.21). CONCLUSIONS: In patients with type 1 diabetes, glucose uptake to the pancreas is enhanced at or soon after the time of diagnosis.

An autoradiographic study of [(18)F]FDG uptake to islets of Langerhans in NOD mouse.

To evaluate the potential of in vivo imaging of accumulation of lymphocytes to islets of Langerhans (insulitis), we compared 2-[(18)F]fluoro-2-deoxy-d-glucose ([(18)F]FDG) uptake in the pancreas and pancreatic islets of healthy BALB/c mice, phenotypically healthy NOD mice with insulitis and diabetic NOD mice. [(18)F]FDG was injected i.v. to 14 female BALB/c mice (age 13+/-3 weeks, plasma glucose 8+/-2 mmol/l) and 21 age-matched female NOD mice (plasma glucose 8+/-4 mmol/l, p=0.06). The mice were killed 90-min post injection and distribution of radioactivity was analysed using digital autoradiography. There was no correlation of plasma glucose concentration with the [(18)F]FDG uptake values. Uptake of radioactivity in NOD mice to the islets affected by insulitis was up to 2.3 times higher (p=0.001) than that to unaffected islets in the same pancreas. Uptake to NOD islets with insulitis was also clearly enhanced (1.0-2.3 times higher) compared to the islets in the BALB/c mice. In conclusion, NOD mouse islets with insulitis accumulate [(18)F]FDG markedly more than islets without insulitis or BALB/c islets. However, the relatively small difference in the [(18)F]FDG intensity between healthy and diseased islets, combined with the limited resolution ability of the positron emission tomography (PET), probably prevent the use of [(18)F]FDG in PET studies aiming at in vivo documentation of onset and progression of insulitis and prediabetes in mouse and man.