Breakdown of the interlayer coherence in twisted bilayer graphene

Coherent motion of the electrons in the Bloch states is one of the fundamental concepts of the charge conduction in solid state physics. In layered materials, however, such a condition often breaks down for the interlayer conduction, when the interlayer coupling is significantly reduced by e.g. large interlayer separation. We report that complete suppression of coherent conduction is realized even in an atomic length scale of layer separation in twisted bilayer graphene. The interlayer resistivity of twisted bilayer graphene is much higher than the c-axis resistivity of Bernal-stacked graphite, and exhibits strong dependence on temperature as well as on external electric fields. These results suggest that the graphene layers are significantly decoupled by rotation and incoherent conduction is a main transport channel between the layers of twisted bilayer graphene.Comment: 5 pages, 3 figure

Chlorin e6 Prevents ADP-Induced Platelet Aggregation by Decreasing PI3K-Akt Phosphorylation and Promoting cAMP Production

A number of reagents that prevent thrombosis have been developed but were found to have serious side effects. Therefore, we sought to identify complementary and alternative medicinal materials that are safe and have long-term efficacy. In the present studies, we have assessed the ability of chlorine e6 (CE6) to inhibit ADP-induced aggregation of rat platelets and elucidated the underlying mechanism. CE6 inhibited platelet aggregation induced by 10 µM ADP in a concentration-dependent manner and decreased intracellular calcium mobilization and granule secretion (i.e., ATP and serotonin release). Western blotting revealed that CE6 strongly inhibited the phosphorylations of PI3K, Akt, c-Jun N-terminal kinase (JNK), and different mitogen-activated protein kinases (MAPKs) including extracellular signal-regulated kinase 1/2 (ERK1/2) as well as p38-MAPK. Our study also demonstrated that CE6 significantly elevated intracellular cAMP levels and decreased thromboxane A2 formation in a concentration-dependent manner. Furthermore, we determined that CE6 initiated the activation of PKA, an effector of cAMP. Taken together, our findings indicate that CE6 may inhibit ADP-induced platelet activation by elevating cAMP levels and suppressing PI3K/Akt activity. Finally, these results suggest that CE6 could be developed as therapeutic agent that helps prevent thrombosis and ischemia

Endoscopic Pancreatic Sphincterotomy: Indications and Complications

Background/Aims: Although a few recent studies have reported the effectiveness of endoscopic pancreatic sphincterotomy (EPST), none has compared physicians' skills and complications resulting from the procedure. Thus, we examined the indications, complications, and safety of EPST performed by a single physician at a single center. Methods: Among 2,313 patients who underwent endoscopic retrograde cholangiopancreatography between January 1996 and March 2008, 46 patients who underwent EPST were included in this retrospective study. We examined the indications, complications, safety, and effectiveness of EPST, as well as the need for a pancreatic drainage procedure and the concomitant application of EPST and endoscopic sphincterotomy (EST). Results: Diagnostic indications for EPST were chronic pancreatitis (26 cases), pancreatic divisum (4 cases), and pancreatic cancer (8 cases). Therapeutic indications for EPST were removal of a pancreaticolith (10 cases), stent insertion for pancreatic duct stenosis (9 cases), nasopancreatic drainage (7 cases), and treatment of sphincter of Oddi dysfunction (1 case). The success rate of EPST was 95.7% (44/46). Acute complications of EPST included five cases (10.9%) of pancreatitis and one of cholangitis (2.2%). EPST with EST did not reduce biliary complications. Endoscopic pancreatic drainage procedures following EPST did not reduce pancreatic complications. Conclusions: EPST showed a low incidence of complications and a high rate of treatment success; thus, EPST is a relatively safe procedure that can be used to treat pancreatic diseases. Pancreatic drainage procedures and additional EST following EPST did not reduce the incidence of procedure-related complications

KCHO-1, a Novel Antineuroinflammatory Agent, Inhibits Lipopolysaccharide-Induced Neuroinflammatory Responses through Nrf2-Mediated Heme Oxygenase-1 Expression in Mouse BV2 Microglia Cells

The brain is vulnerable to oxidative stress and inflammation that can occur as a result of aging or neurodegenerative diseases. Our work has sought to identify natural products that regulate heme oxygenase (HO)-1 and to determine their mechanism of action in neurodegenerative diseases. KCHO-1 is a novel herbal therapeutic containing 30% ethanol (EtOH) extracts from nine plants. In this study, we investigated the antineuroinflammatory effects of KCHO-1 in lipopolysaccharide- (LPS-) treated mouse BV2 microglia. KCHO-1 inhibited the protein expression of inducible nitric oxide synthase (iNOS), iNOS-derived nitric oxide (NO), cyclooxygenase- (COX-) 2, and COX-2-derived prostaglandin E2 (PGE2) in LPS-stimulated BV2 microglia. It also reduced tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 production. This effect was correlated with the suppression of inhibitor of nuclear factor kappa B-α (IκB-α) phosphorylation and degradation and nuclear factor kappa B (NF-κB) translocation and DNA binding. Additionally, KCHO-1 upregulated HO-1 expression by promoting nuclear translocation of nuclear factor E2-related factor 2 (Nrf2) in mouse BV2 microglia. Tin protoporphyrin (SnPP), an HO activity inhibitor, was used to verify the inhibitory effects of KCHO-1 on proinflammatory mediators and proteins associated with HO-1 expression. Our data suggest that KCHO-1 has therapeutic potential in neurodegenerative diseases caused by neuroinflammation

Multimodal MRI-Based Triage for Acute Stroke Therapy: Challenges and Progress

Revascularization therapies have been established as the treatment mainstay for acute ischemic stroke. However, a substantial number of patients are either ineligible for revascularization therapy, or the treatment fails or is futile. At present, non-contrast computed tomography is the first-line neuroimaging modality for patients with acute stroke. The use of magnetic resonance imaging (MRI) to predict the response to early revascularization therapy and to identify patients for delayed treatment is desirable. MRI could provide information on stroke pathophysiologies, including the ischemic core, perfusion, collaterals, clot, and blood–brain barrier status. During the past 20 years, there have been significant advances in neuroimaging as well as in revascularization strategies for treating patients with acute ischemic stroke. In this review, we discuss the role of MRI and post-processing, including machine-learning techniques, and recent advances in MRI-based triage for revascularization therapies in acute ischemic stroke