Differences in Treatment Effects of Cognitive-behavioral Therapy for Insomnia Based on Sleep Reactivity: A Preliminary Study.

INTRODUCTION: Sleep reactivity is the trait-like degree to which stress disrupts sleep, resulting in difficulty falling and staying asleep. Although previous studies have suggested that individuals who have high sleep reactivity may be resistant to cognitive-behavioral therapy for insomnia (CBT-I) effects, there have been no studies that have investigated this empirically. This study explored differential treatment responses in CBT-I based on sleep reactivity levels. MATERIAL AND METHOD: Participants for this study were nineteen insomnia patients who met DSM-5 criteria for insomnia disorder. All participants received four weekly sessions of structured cognitive-behavioral therapy for insomnia (CBT-I). Individuals completed the Insomnia Severity Index (ISI), Korean version of Center for Epidemiologic Studies Depression Scale-Revised (K-CESD-R), Ford Insomnia Response to Stress Test (FIRST), Dysfunctional Beliefs and Attitudes about Sleep Scale-16 (DBAS-16), the Daily Inventory of Stressful Events (DISE) and a sleep diary. Participants were classified into two groups based on sleep reactivity level (high and low sleep reactivity). RESULT: Following treatment, significant changes were found for ISI, K-CESD-R, DBAS-16 and FIRST scores, sleep onset latency, wake after sleep onset, sleep efficiency, number of awakenings, sleep quality and feeling refreshed upon awakening in both groups. Improvements in sleep efficiency was lower in the high sleep reactivity group compared to the low sleep reactivity group. No differences in ISI, K-CESD-R, DBAS-16 scores, and stress event frequency during the treatment duration were found between groups. CONCLUSION: These findings suggest that sleep reactivity level may be an important factor that affects treatment outcome of CBT-I. Furthermore, the results may suggest that individual response to stress events are more important than the stressor itself.

Transcallosal fibers from corticospinal tract in patients with cerebral infarct.

Diffusion tensor image tractography (DTT) can visualize white matter tracts and provide a powerful vehicle with which to investigate the neural pathway at the subcortical level. We attempted to demonstrate the clinical significance of transcallosal fibers (TCF) originating from the corticospinal tract in patients with corona radiata infarct located below the corpus callosum, using diffusion tensor image tractography (DTT). Forty patients with corona radiata infarct located below the corpus callosum and 26 control subjects were enrolled in this study. We classified the DTT findings as follows: no transcallosal fiber from the CST (type A), transcallosal fiber ended in the corpus callosum or connected to the cortex of the opposite hemisphere (type B), and transcallosal fiber that descended toward the lesion after passing through the corpus callosum (type C). Type C indicated that the presence of transcallosal fibers starting from the CST of the unaffected hemisphere was significantly more prevalent in the patients, and these patients showed the poorest motor function. It seems that transcallosal fibers originated from the CST of the unaffected hemisphere, and fibers descending toward the lesion in patients with corona radiata infarct may act to compensate for motor deficits.

Sphingosine 1-phosphate induces vascular endothelial growth factor expression in endothelial cells.

Angiogenesis is essential for tumor growth and vascular endothelial cell growth factor (VEGF) plays a key role in this process. Conversely, sphingosine 1-phosphate (S1P) is a biologically active sphingolipid known to play a key role in cancer progression by regulating endothelial cell proliferation and migration. In this study, the authors found that S1P increases the level of VEGF mRNA in human umbilical vein endothelial cells (HUVECs) and immortalized HUVECs (iHUVECs). Additionally, S1P was found to increase VEGF promoter activity in MS-1 mouse pancreatic islet endothelial cells. Furthermore, a pharmacological inhibitory study revealed that G(alpha i/o)-mediated phospholipase C, Akt, Erk, and p38 MAPK signaling are involved in this S1P-induced expression of VEGF. A component of AP1 transcription factor is important for S1P-induced VEGF expression. Taken together, these findings suggest that S1P enhances endothelial cell proliferation and migration by upregulating the expression of VEGF mRNA.