Extracting laboratory test information from biomedical text

Background: No previous study reported the efficacy of current natural language processing (NLP) methods for extracting laboratory test information from narrative documents. This study investigates the pathology informatics question of how accurately such information can be extracted from text with the current tools and techniques, especially machine learning and symbolic NLP methods. The study data came from a text corpus maintained by the U.S. Food and Drug Administration, containing a rich set of information on laboratory tests and test devices. Methods: The authors developed a symbolic information extraction (SIE) system to extract device and test specific information about four types of laboratory test entities: Specimens, analytes, units of measures and detection limits. They compared the performance of SIE and three prominent machine learning based NLP systems, LingPipe, GATE and BANNER, each implementing a distinct supervised machine learning method, hidden Markov models, support vector machines and conditional random fields, respectively. Results: Machine learning systems recognized laboratory test entities with moderately high recall, but low precision rates. Their recall rates were relatively higher when the number of distinct entity values (e.g., the spectrum of specimens) was very limited or when lexical morphology of the entity was distinctive (as in units of measures), yet SIE outperformed them with statistically significant margins on extracting specimen, analyte and detection limit information in both precision and F-measure. Its high recall performance was statistically significant on analyte information extraction. Conclusions: Despite its shortcomings against machine learning methods, a well-tailored symbolic system may better discern relevancy among a pile of information of the same type and may outperform a machine learning system by tapping into lexically non-local contextual information such as the document structure

Spin dependence of the magnetization step in the Pr-doped manganites

Magnetic measurements were performed to study a single crystal Pr0.5Sr0.5MnO3 and polycrystalline Pr0.6Ca0.4MnO3. Magnetic-field$\hbox{--}$induced magnetization step is observed at low temperature for Pr-doped phase-separated manganites. Magnetization measurements indicate that the spin-stiffness constant D exhibits large magnetic-field dependence. Moreover, there exists a remarkable change of the spin-stiffness constant corresponding to the variety of the step-like magnetization. Our results suggest that the spin-wave inherent to the coexistence of the antiferromagnetic and ferromagnetic phases plays a crucial role in the mechanism of these magnetic transformations

Metformin attenuates myocardial ischemia-reperfusion injury via up-regulation of antioxidant enzymes

<div><p>The objective was to examine the protective effect of metformin (Met) on myocardial ischemia-reperfusion (IR) injury and whether the mechanism was related to the AMPK/ antioxidant enzymes signaling pathway. Rat Langendorff test and H₂O₂-treated rat cardiomyocytes (H9c2) were used in this study. Met treatment significantly improved left ventricular (LV) function, reduced infarct size and CK-MB release in comparison with IR group. Decreased TUNEL staining positive cells were also observed in IR+Met group <i>ex vivo</i>. Met treatment markedly inhibited IR inducing cell death and significantly decreased apoptosis with few generations of reactive oxygen species (ROS) in H9c2 cells in comparison with IR group. Up-regulated expressions of phosphorylated LKB1/AMPK/ACC, as well as down-regulated expressions of apoptotic proteins (Bax and cleaved caspase 3) were found in IR+Met group when compared to the IR group. Importantly, Met significantly up-regulated the expression of antioxidant enzymes (MnSOD and catalase) during IR procedure either <i>ex vivo</i> or <i>in vitro</i>. Compound C, a conventional inhibitor of AMPK, abolished the promoting effect of Met on antioxidant enzymes, and then attenuated the protective effect of Met on IR injury <i>in vitro</i>. In conclusion, Met exerted protective effect on myocardial IR injury, and this effect was AMPK/ antioxidant enzymes dependent.</p></div

The effect of Met on AMPK signaling pathway, antioxidant enzymes and apoptosis <i>ex vivo</i>.

<p>The protein levels of LKB1/AMPK/ACC were determined (A). Protein levels of MnSOD, mRNA levels of MnSOD and catalase were determined (B). Akt, Bax, cleaved caspase-3 protein levels were examined (C). TUNEL staining was performed to further confirm apoptosis; apoptotic cells were stained with brown color. The black line represented a scale bar of 50μm (D). *p<0.05 vs. Con group, #p<0.05 vs. IR group.</p

The effect of Met on cell death and AMPK signaling pathway <i>in vitro</i>.

<p>Calcein AM/PI double staining was performed in H9c2 cells to determine cell death (A). Quantification of survived cells rate was calculated (B). The protein levels of AMPK/ACC were determined in H9c2 cells (C). *p<0.05 vs. Con group, #p<0.05 vs. IR group, & p<0.05 vs. IR+Met group, $ p<0.05 vs. IR+AICAR group.</p

The effect of Met on left ventricular function during myocardial IR.

<p>LVDP, LVEDP and ± dp/dt max were recorded and calculated in Langendoff perfusion test. No significant differences were found between 3 groups in stabilization period. Left ventricular function was decreased in reperfusion period whereas Met treatment significantly increased left ventricular function. *p<0.05 vs. Con group, #p<0.05 vs. IR group. n = 6–8 rats/group.</p

The effect of Met on apoptosis during IR in H9c2 cells.

<p>Apoptotic cells were defined as the Annexin V-FITC positive cells (cells in Q2 and Q3). *p<0.05 vs. Con group, #p<0.05 vs. IR group, & p<0.05 vs. IR+Met group, $ p<0.05 vs. IR+AICAR group.</p

The effect of Met on heart infarct size and CK-MB release.

<p>Heart infarct size was evaluated by TTC staining (A). CK-MB release was measured by ELISA (B). *p<0.05 vs. Con group, #p<0.05 vs. IR group.</p

The effect of Met on apoptosis <i>in vitro</i>.

<p>Hoechst 33342 (for apoptosis) and TMRM (for mitochondrial ΔΨm) double staining was performed (A). Akt, Bax, cleaved caspase-3 protein levels were examined in H9c2 cells (B). *p<0.05 vs. Con group, #p<0.05 vs. IR group, & p<0.05 vs. IR+Met group, $ p<0.05 vs. IR+AICAR group.</p