Evaluating the performance of whole genome amplification for use in low template DNA typing.

We report on the performance of two whole genome amplification methods, GenomiPhi™ amplification and modified-improved primer extension preamplification (mIPEP), when analysing low template DNA samples. Template as low as 10 pg treated with mIPEP generated more than 1 ng of DNA that could be used in STR typing. Initial templates of 100-10 pg, when treated with mIPEP, generated an increase in alleles compared with control samples. Partial profiles using the AmpFℓSTR(®) Identifiler™ Kit were produced from this suboptimal DNA template, with 70% of the possible alleles (21.7 ± 2.1 in 32 alleles) recorded, using the mIPEP amplified products with an initial template of 100 pg. Allelic imbalance decreased with samples treated with whole genome amplification method (WGA) compared with those without this initial treatment. Further methods for improvement were also analysed including altering the condition of electrokinetic injection, and the successful DNA typing rate was increased to about 80%. This report illustrates the potential use and limitations of WGA for low template samples.

The Use of Neuroimaging for Predicting Sumatriptan Treatment Response in Patients With Migraine.

OBJECTIVES: To identify the neuroimaging predictors for the responsiveness of patients to sumatriptan and use an independent cohort for external validation. METHODS: Structuralized headache questionnaire and 3-Tesla brain magnetic resonance imaging were performed in migraine patients. Regional brain volumes were automatically calculated using FreeSurfer version 6.0, including bilateral amygdala, anterior cingulated cortex, caudate, putamen, precuneus, orbitofrontal cortex, superior frontal gyri, middle frontal gyri, hippocampus, and parahippocampus. A sumatriptan-responder was defined as headache relief within 2 h after the intake of sumatriptan in at least two out of three treated attacks. We constructed a prediction model for sumatriptan response using the regional brain volume and validated it with an independent cohort of migraine patients. RESULTS: A total of 105 migraine patients were recruited, including 73 sumatriptan responders (69.5%) and 32 (30.5%) non-responders. We divided the migraine patients into derivation (n = 73) and validation cohorts (n = 32). In the derivation cohort, left hippocampal volume was larger in sumatriptan responders (responders vs. non-responders: 3,929.5 ± 403.1 vs. 3,611.0 ± 389.9 mm3, p = 0.002), and patients with a larger left hippocampal volume had a higher response rate to sumatriptan (>4,036.2 vs. ≤4,036.2 mm3: 92.0 vs. 56.3%, p = 0.001). Based on the findings, we constructed a prediction model using the cutoff value of 4,036.2 mm3, and we found that patients with a left hippocampal volume >4,032.6 mm3 had a higher response rate to sumatriptan than those with a left hippocampal volume ≤4,032.6 mm3 (84.6 vs. 42.1%, odds ratio [OR] = 7.6 [95% confidence interval = 1.3-44.0], p = 0.013) in the validation cohort. CONCLUSION: Our study showed that left hippocampal volume is helpful to identify sumatriptan non-responders. This proof-of-concept study shows that left hippocampal volume could be used to predict the treatment response to sumatriptan in migraine patients.