Mild traumatic brain injury is associated with effect of inflammation on structural changes of default mode network in those developing chronic pain
JOURNAL OF HEADACHE AND PAIN
Authors: Niu, Xuan; Bai, Lijun; Sun, Yingxiang; Wang, Yuan; Bai, Guanghui; Yin, Bo; Wang, Shan; Gan, Shuoqiu; Jia, Xiaoyan; Liu, Hongjuan
Abstract
Background: Mild traumatic brain injury (mTBI) has a higher prevalence (more than 50%) of developing chronic posttraumatic headache (CPTH) compared with moderate or severe TBI. However, the underlying neural mechanism for CPTH remains unclear. This study aimed to investigate the inflammation level and cortical volume changes in patients with acute PTH (APTH) and further examine their potential in identifying patients who finally developed CPTH at follow-up. Methods: Seventy-seven mTBI patients initially underwent neuropsychological measurements, 9-plex panel of serum cytokines and MRI scans within 7 days post-injury (T-1) and 54 (70.1%) of patients completed the same protocol at a 3-month follow-up (T-2). Forty-two matched healthy controls completed the same protocol at T-1 once. Results: At baseline, mTBI patients with APTH presented significantly increased GM volume mainly in the right dorsal anterior cingulate cortex (dACC) and dorsal posterior cingulate cortex (dPCC), of which the dPCC volume can predict much worse impact of headache on patients' lives by HIT-6 (beta = 0.389, P = 0.007) in acute stage. Serum levels of C-C motif chemokine ligand 2 (CCL2) were also elevated in these patients, and its effect on the impact of headache on quality of life was partially mediated by the dPCC volume (mean [SE] indirect effect, 0.088 [0.0462], 95% CI, 0.01-0.164). Longitudinal analysis showed that the dACC and dPCC volumes as well as CCL2 levels had persistently increased in patients developing CPTH 3 months postinjury. Conclusion: The findings suggested that structural remodelling of DMN brain regions were involved in the progression from acute to chronic PTH following mTBI, which also mediated the effect of inflammation processes on pain modulation.
The conditioning role of performance on the bank risk-taking channel of monetary policy: Evidence from a multiple-tool regime
RESEARCH IN INTERNATIONAL BUSINESS AND FINANCE
Authors: Van Dan Dang; Van Cuong Dang
Abstract
The study investigates how monetary policy affects bank risk-taking under a multiple-tool regime of Vietnam during 2007-2018. Particularly, we also consider the conditioning role of bank performance, broken down by bank profitability and cost efficiency, in this nexus. Using both dynamic and static panel models, we show that the liquidity injection initiated by the central bank's asset purchases induces banks to take more risks, captured by the traditional Z-score and two alternative measures of credit risk. However, monetary policy easing through decreased interest rates is beneficial to the credit portfolio and financial stability of banks, which therefore challenges the functioning of the bank risk-taking channel. This startling result is robust across three different interest rate measures, including lending rates, refinance rates and rediscount rates. Further analysis reveals that our observed effects are alleviated for banks with higher performance - i.e., more profitable and efficient banks. This in-depth finding offers more in-sights into the "search for yield" incentive, based on the theory of information asymmetry and the two competing hypotheses of "bad management" and "cost skimping".