Purpose To determine the correlation between diffusion kurtosis imaging (DKI)-derived parameters and prognostic factors for rectal adenocarcinoma. Materials and Methods This study was approved by the local institute review board, and written informed consent was obtained from each patient. Data from 56 patients (median age, 59.5 years; age range, 31-86 years) with rectal adenocarcinoma between April 2014 and September 2015 were involved in this prospective study. DKI (b = 0, 700, 1400, and 2100 sec/mm) and conventional diffusion-weighted imaging (b = 0, 1000 sec/mm) were performed. Kurtosis and diffusivity from DKI and apparent diffusion coefficients (ADCs) from diffusion-weighted imaging were measured by two radiologists. Student t test, receiver operating characteristic curves, and Spearman correlation were used for statistical analysis. Results Kurtosis was significantly higher in high-grade than in low-grade rectal adenocarcinomas on the basis of both the number of poorly differentiated clusters (PDCs) (1.136 ± 0.086 vs 0.988 ± 0.060, P < .05) and World Health Organization (WHO) grades (1.103 ± 0.086 [standard deviation] vs 1.034 ± 0.103, P < .05). In PDC grading, the diffusivity and ADC were significantly lower in high-grade tumors than in low-grade tumors (1.187 ± 0.150 vs 1.306 ± 0.129 and 1.020 ± 0.113 vs 1.108 ± 0.097, respectively; P < .05) and showed similar correlations with histologic grades (r = -0.486 and r = -0.406, respectively; P > .05). Compared with both diffusivity and ADC, kurtosis showed significantly higher sensitivity (83.3% [20 of 24] vs 70.8% [17 of 24] and 70.8% [17 of 24], respectively) and specificity (96.8% [31 of 32] vs 84.4% [24 of 32] and 81.3% [26 of 32], respectively). Kurtosis showed a better correlation with PDC grades than with WHO grades (r = 0.797 vs r = 0.293, P < .05). Kurtosis was significantly higher in pN1-2 than in pN0 tumors (1.086 ± 0.103 vs 1.009 ± 0.086, P < .05). Conclusion Kurtosis derived from DKI demonstrated a higher correlation with histologic grades compared with diffusivity and ADC. It also showed better performance in differentiating between high- and low-grade rectal adenocarcinomas and between pN1-2 and pN0 tumors. RSNA, 2016.

Summary Background While direct‐acting antivirals have been approved for treating hepatitis C, the guidelines highlight the importance of considering potential drug‐drug interactions between DAAs and concomitant medications. Aim To assess comorbidity prevalence, concomitant medication use and potential drug‐drug interactions between DAAs and concomitant medications for hepatitis C patients in Taiwan. Methods This cross‐sectional study enrolled 822 patients from May to August 2016 in Taiwan. Patient demographics, comorbidities and concomitant medications were evaluated by physician surveys. Results A total of 709 (86.3%) patients had ≥1 comorbidity; the most prevalent comorbidity categories were diseases of the digestive system (40.1%), circulatory system (38.7%) and endocrine/nutritional/metabolic diseases (35.2%). Elderly patients had more comorbidities. A total of 622 (75.7%) patients received ≥1 concomitant medication; the average number of concomitant medications was 3.2. The most common concomitant medication classes were cardiovascular (34.4%), gastrointestinal (25.7%) and central nervous system drugs (22.7%). Among patients without cirrhosis or with compensated cirrhosis, contraindications were most prevalent with paritaprevir/ritonavir/ombitasvir plus dasabuvir, daclatasvir/asunaprevir and glecaprevir/pibrentasvir (13.3%, 6.0% and 5.4% respectively), and least prevalent with sofosbuvir, sofosbuvir/daclatasvir, sofosbuvir/ledipasvir and sofosbuvir/velpatasvir (0.8%, 1.3%, 1.4% and 2.1% respectively). Sofosbuvir‐based regimens had no contraindications in patients with decompensated cirrhosis. Conclusion Our population represented an elderly demographic, with a high prevalence of comorbidities and widespread use of concomitant medications. The potential drug‐drug interactions between these concomitant medications and DAA regimens differed, with the fewest potential interactions with sofosbuvir‐based regimens.

BackgroundTemporal lobe epilepsy (TLE) is one of the most drug-resistant types of epilepsy with about 80% of TLE patients falling into this category. Increasing evidence suggests that neuroinflammation, which has a critical role in the epileptogenesis of TLE, is associated with microglial activation. Therefore, agents that act toward the alleviation in microglial activation and the attenuation of neuroinflammation are promising candidates to treat TLE. α-Asarone is a major active ingredient of the Acori Graminei Rhizoma used in Traditional Chinese Medicine, which has been used to improve various disease conditions including stroke and convulsions. In addition, an increasing number of studies suggested that α-asarone can attenuate microglia-mediated neuroinflammation. Thus, we hypothesized that α-asarone is a promising neuroprotective agent for the treatment of the TLE.MethodsThe present study evaluated the therapeutic effects of α-asarone on microglia-mediated neuroinflammation and neuroprotection in vitro and in vivo, using an untreated control group, a status epilepticus (SE)-induced group, and an SE-induced α-asarone pretreated group. A pilocarpine-induced rat model of TLE was established to investigate the neuroprotective effects of α-asarone in vivo. For the in vitro study, lipopolysaccharide (LPS)-stimulated primary cultured microglial cells were used.ResultsThe results indicated that the brain microglial activation in the rats of the SE rat model led to important learning and memory deficit. Preventive treatment with α-asarone restrained microglial activation and reduced learning and memory deficit. In the in vitro studies, α-asarone significantly suppressed proinflammatory cytokine production in primary cultured microglial cells and attenuated the LPS-stimulated neuroinflammatory responses. Our mechanistic study revealed that α-asarone inhibited inflammatory processes by regulation the transcription levels of kappa-B, by blocking the degradation pathway of kappa B-alpha [inhibitor kappa B-alpha (IκB-α)] and kappa B-beta (IκB-β) kinase in both the SE rats and in primary cultured microglial cells.ConclusionTaken together, these data demonstrate that α-asarone is a promising neuroprotective agent for the prevention and treatment of microglia-mediated neuroinflammatory conditions including TLE, for which further assessment studies are pertinent.