Diagnostic Value of Serum Amylase Levels Indicating Computed Tomography-Defined Post-Endoscopic Retrograde Cholangiopancreatography Pancreatitis: A Prospective Multicenter Observational Study.

Objective:Post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis involves persistent serum amylase levels of 3 times or more the standard upper limit. However, these criteria were mostly based on retrospective studies and not necessarily supported by diagnostic imaging. Our prospective study aimed to investigate cutoff serum amylase levels suggesting post-ERCP pancreatitis using computed tomography as the criterion standard.Methods:We prospectively followed 2078 cases. Computed tomography was performed in patients whose serum amylase levels exceeded the institutional upper limit 12 to 24 hours after ERCP. Two expert radiologists blindly assessed the images and judged the presence or absence of pancreatitis. Correlations between serum amylase levels with pancreatitis were investigated using receiver operating characteristic analysis.Results:Amylase levels increased in 416 (23.2%) of 1789 cases included, and 350 cases were analyzed using computed tomography. Post-endoscopic retrograde cholangiopancreatography pancreatitis was diagnosed in 12.0% (214/1789). The cutoff amylase levels for judging pancreatitis after 12 to 24 hours was 2.75 times higher than the institutional upper limit, with an area under the curve of 0.77.Conclusions:The appropriate cutoff serum amylase level for judging post-ERCP pancreatitis at 12 to 24 hours after ERCP was 2.75 times higher than the institutional upper limit. These results may clarify the definition of post-ERCP pancreatitis

Emission wavelength dependence of internal quantum efficiency in InGaN nanowires

The internal quantum efficiency (IQE) of InGaN nanowires with different emission wavelength of 485, 515, 555, and 580 nm has been studied by means of photoluminescence (PL) spectroscopy. It was found from the analysis of IQE as a function of excitation power density that the IQE was unchanged at about 100% under weak excitation conditions at low temperature. This indicated that the effects of nonradiative recombination processes were negligibly small at low temperature. Moreover, the IQE increased from 5 to 12% with increasing emission wavelength from 485 to 580 nm. Since the clear correlation between the IQE and the PL blue shift due to band filling effects of localized states was observed, the increase in the IQE reflected the increase in the effect of exciton localization with increasing indium composition. </jats:p

The Secretogranin II Gene Is a Signal Integrator of Glutamate and Dopamine Inputs

Cooperative gene regulation by different neurotransmitters likely underlies the long-term forms of associative learning and memory, but this mechanism largely remains to be elucidated. Following cDNA microarray analysis for genes regulated by Ca(2+) or cAMP, we found that the secretogranin II gene (Scg2) was cooperatively activated by glutamate and dopamine in primary cultured mouse hippocampal neurons. The Ca(2+) chelator BAPTA-AM and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059 prevented Scg2 activation by glutamate or dopamine; thus, the Ca(2+) /MEK pathway is predicted to include a convergence point(s) of glutamatergic and dopaminergic signaling. Unexpectedly, the protein kinase A (PKA) inhibitor KT5720 enhanced Scg2 activation by dopamine. The protein-synthesis inhibitor cycloheximide also enhanced Scg2 activation, and the proteasome inhibitor ZLLLH diminished the KT5720-mediated augmentation of Scg2 activation. These results are concordant with the notion that dopaminergic input leads to accumulation of a KT5720-sensitive transcriptional repressor, which is short-lived because of rapid degradation by proteasomes. This repression pathway may effectively limit the time window permissive to Scg2 activation by in-phase glutamate and dopamine inputs via the Ca(2+) /MEK pathway. We propose that the regulatory system of Scg2 expression is equipped with machinery that is refined for the signal integration of in-phase synaptic inputs. This article is protected by copyright. All rights reserved