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In addition, the stress and rest summed segmental scores were calculated using a 17-segment model with each segment scored from 0 to 4 (0 normal, 1 mild, 2 moderate, 3 severe defect and 4 absent tracer uptake).
Each segment scored as 0 = normal, 1 = mild hypokinesia, 2 = severe hypokinesia, 3 = akinesia, or 4 = dyskinesia.
Because three-base periodicities identified as G-hits do not provide information on the reading frame and coding strand of a potential gene, G-hits were re-scored, as for the H-hits, by H-scores against coding in alternative frames (see earlier), and retained only if the G-value of the final high-scoring segment scored significantly by the G-test.
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WMSI was defined as the total of the wall motion scores divided by the number of segments scored.
The first-order segments receive a score of 1 and the second order segments scored 0.5.
An "extent of disease" score was obtained by counting the number of bronchopulmonary segments involved for each abnormality: one to three segments scored as 1; four to nine segments scored as 2; more than nine segments scored as 3.
A 16-segment LVWMI (left ventricular wall motion index) based on the American Society of Echocardiography mode was derived by scoring each LV segment [1=normal, 2=hypokinesis, 3=akinesis and 4=dyskinesis (paradoxical motion)] and dividing the total by the number of segments scored.
Semiquantitative scoring was derived from streaking and diluting the specimen in three segments, scored as few for less than 10 colonies, light, moderate and heavy growth when moderate to heavy growth was observed in first, second and third streaks respectively.
The presence or absence of regional wall motion abnormalities (WMA) was assessed by using the 16-segments scoring model proposed by the American Society of Echocardiography (1 = normal wall motion, 2 = hypokinesia, 3 = akinesia).
This was repeated 10,000 times to obtain the distribution of the highest-scoring genome wide segment score.
The results showed a strong signal for this DNA segment that scored higher than the DNA segment in intron 1, whereas a control segment at the 3' end of the Col2a1 gene gave no signal (Figure S4).
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