(Methanol-κO)(perchlorato-κO)bis­(triphenyl­phosphine-κP)silver(I)

In the title complex, [Ag(ClO4)(CH3OH)(C18H15P)2], the angles around the central Ag+ ion indicate that it is in a distorted tetrahedral coordination. The coordination sphere of silver is formed by two P atoms of two triphenyl­phosphine ligands, one O atom of a perchlorate anion and one O atom of a methanol mol­ecule. The crystal structure is stablized by a bifurcated inter­molecular O—H⋯O hydrogen bond, involving the O—H donor from methanol and two acceptor O atoms from the perchlorate anion, so forming a zigzag chain propagating in [010]

Tetra­kis(triphenyl­phosphane-κP)silver(I) trifluoro­methane­sulfonate dichloro­methane monosolvate

In the title compound, [Ag(C18H15P)4]CF3O3S·CH2Cl2, the Ag atom is coordinated by four P atoms from four PPh3 ligands. The P—Ag—P angles are in the range 108.02 (6)–110.15 (6)°, which confirms the distorted tetra­hedral environment around the Ag atom

Policosanol Attenuates Statin-Induced Increases in Serum Proprotein Convertase Subtilisin/Kexin Type 9 When Combined with Atorvastatin

Objective. Statin treatment alone has been demonstrated to significantly increase plasma proprotein convertase subtilisin/kexin type 9 (PCSK9) levels. The effect of policosanol combined with statin on PCSK9 is unknown. Methods. Protocol I: 26 patients with atherosclerosis were randomly assigned to receive either atorvastatin 20 mg/d or policosanol 20 mg/d + atorvastatin 20 mg/d for 8 weeks. Protocol II: 15 healthy volunteers were randomly assigned to either policosanol 20 mg/d or a control group for 12 weeks. Serum levels of PCSK9 were determined at day 0 and the end of each protocol. Results. Protocol I: atorvastatin 20 mg/d significantly increased serum PCSK9 level by 39.4% (256 ± 84 ng/mL versus 357 ± 101 ng/mL, P=0.002). However, policosanol 20 mg/d + atorvastatin 20 mg/d increased serum PCSK9 level by only 17.4% without statistical significance (264 ± 60 ng/mL versus 310 ± 86 ng/mL, P=0.184). Protocol II: there was a trend toward decreasing serum PCSK9 levels in the policosanol group (289 ± 71 ng/mL versus 235 ± 46 ng/mL, P=0.069). Conclusion. Policosanol combined with statin attenuated the statin-induced increase in serum PCSK9 levels. This finding indicates that policosanol might have a modest effect of lowering serum PCSK9 levels

Impaired Cognitive Function and Altered Hippocampal Synaptic Plasticity in Mice Lacking Dermatan Sulfotransferase Chst14/D4st1

Chondroitin sulfate (CS) and dermatan sulfate (DS) proteoglycans (PGs) are major extracellular matrix (ECM) components of the central nervous system (CNS). A large body of evidence has shown that CSPGs/DSPGs play critical roles in neuronal growth, axon guidance, and plasticity in the developing and mature CNS. It has been proposed that these PGs exert their function through specific interaction of CS/DS chains with its binding partners in a manner that depends on the sulfation patterns of CS/DS. It has been reported that dermatan 4-O-sulfotransferase-1 (Chst14/D4st1) specific for DS, but not chondroitin 4-O-sulfotransferase-1 (Chst11/C4st1) specific for CS, regulates proliferation and neurogenesis of neural stem cells (NSCs), indicating that CS and DS play distinct roles in the self-renewal and differentiation of NSCs. However, it remains unknown whether specific sulfation profiles of DS has any effect on CNS plasticity. In the present study, Chst14/D4st1-deficient (Chst14−/−) mice was employed to investigate the involvement of DS in synaptic plasticity. First, behavior study using Morris Water Maze (MWM) showed that the spatial learning and memory of Chst14−/− mice was impaired when compared to their wild type (WT) littermates. Corroborating the behavior result, long-term potentiation (LTP) at the hippocampal CA3-CA1 connection was reduced in Chst14−/− mice compared to the WT mice. Finally, the protein levels of N-Methyl-D-aspartate (NMDA) receptor, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor, postsynaptic density 95 (PSD95), growth associated protein 43 (GAP-43), synaptophysin (SYN) and N-ethylmaleimide sensitive factor (NSF) which are important in synaptic plasticity were examined and Chst14/D4st1 deficiency was shown to significantly reduce the expression of these proteins in the hippocampus. Further studies revealed that Akt/mammalian target rapamycin (mTOR) pathway proteins, including protein kinase B (p-Akt), p-mTOR and p-S6, were significantly lower in Chst14−/− mice, which might contribute to the decreased protein expression. Together, this study reveals that specific sulfation of DS is critical in synaptic plasticity of the hippocampus and learning and memory, which might be associated with the changes in the expression of glutamate receptors and other synaptic proteins though Akt/mTOR pathway

Increased red cell distribution width in patients with slow coronary flow syndrome

OBJECTIVE: An elevated red cell distribution width has been recognized as a predictor of various cardiovascular diseases. Slow coronary flow syndrome is an important angiographic clinical entity with an unknown etiology. This study aimed to examine the relationship between red cell distribution width and the presence of slow coronary flow syndrome. METHODS: In total, 185 patients with slow coronary flow syndrome and 183 age- and gender-matched subjects with normal coronary flow (controls) were prospectively enrolled in this study. Red cell distribution width and C-reactive protein were measured upon admission, and the results were compared between the patients with slow coronary flow syndrome and normal controls. RESULTS: Red cell distribution width levels were significantly higher in the patients with slow coronary flow syndrome than the normal controls. Moreover, the data showed that the plasma C-reactive protein levels were also higher in the patients with slow coronary flow syndrome than in the normal controls. In addition, a multivariate analysis indicated that C-reactive protein and red cell distribution width were the independent variables most strongly associated with slow coronary flow syndrome. Finally, the red cell distribution width was positively correlated with C-reactive protein and mean thrombosis in the myocardial infarction frame counts of the patients with slow coronary flow syndrome. CONCLUSION: The data demonstrated that red cell distribution width levels are significantly higher and strongly positively correlated with both C-reactive protein and thrombosis in the myocardial infarction frame counts of patients with slow coronary flow syndrome. These findings suggest that red cell distribution width may be a useful marker for patients with slow coronary flow syndrome

Evaluation of red blood cell distribution width in patients with cardiac syndrome X

Abstract. BACKGROUND: Cardiac syndrome X (CSX) is a condition characterized by chest pain with normal coronary arteries. However, its pathogenesis has not fully been understood yet. Red blood cell distribution width (RDW) has recently been suggested as a marker of acute and chronic cardiovascular diseases, while no data is available in patients with CSX. METHODS: One hundred and twenty consecutive patients with CSX and 102 normal controls were prospectively enrolled in this study. Blood samples were drawn from all individuals for measuring RDW and high-sensitivity C-reactive protein (CRP). The baseline data were compared between patients with CSX and normal controls. RESULTS: The RDW levels were significantly higher in patients with CSX than that in those with normal controls (13.1 ± 2.1 versus 12.3 ± 1.8, p = 0.011). Moreover, the data showed that the levels of plasma CRP were marked higher in patients with CSX than those that were observed in normal controls (CRP: 2.8 ± 2.2 mg/L versus 2.0 ± 1.7 mg/dl, p = 0.014). In addition, the multivariate analysis indicated that peripheral monocyte cell, CRP and RDW were the independent variables most strongly associated with CSX. In a receiver operating characteristic (ROC) curve analysis, we found that an RDW value of 12.8% was used as an effective cut-point in the segregation of the presence or absence of cardiac syndrome X, a sensitivity of 52.0% and a specificity of 65.4% were obtained. Finally, correlation analysis suggested that there was positive correlation between plasma levels of CRP and RDW levels (n = 120, γ = 0.381, P = 0.013). CONCLUSIONS: The present study, for the first time, demonstrated that elevated RDW and CRP levels were independently associated with the presence of CSX

Suppression of microRNA-222-3p ameliorates ulcerative colitis and colitis-associated colorectal cancer to protect against oxidative stress via targeting BRG1 to activate Nrf2/HO-1 signaling pathway

Oxidative stress is an important pathogenic factor in ulcerative colitis (UC) and colitis-associated colorectal cancer (CAC), further impairing the entire colon. Intestinal epithelial cells (IECs) are crucial components of innate immunity and play an important role in maintaining intestinal barrier function. Recent studies have indicated that microRNA-222-3p (miR-222-3p) is increased in colon of UC and colorectal cancer (CRC) patients, and miR-222-3p is a crucial regulator of oxidative stress. However, whether miR-222-3p influences IEC oxidative stress in UC and CAC remains unknown. This study investigated the effect of miR-222-3p on the regulation of IEC oxidative stress in UC and CAC. An in vitro inflammation model was established in NCM460 colonic cells, mouse UC and CAC models were established in vivo, and IECs were isolated. The biological role and mechanism of miR-222-3p-mediated oxidative stress in UC and CAC were determined. We demonstrated that miR-222-3p expression was notably increased in dextran sulfate sodium (DSS)-induced NCM460 cells and IECs from UC and CAC mice. In vitro, these results showed that the downregulation of miR-222-3p reduced oxidative stress, caspase-3 activity, IL-1β and TNF-α in DSS-induced NCM460 cells. We further identified BRG1 as the target gene of miR-222-3p, and downregulating miR-222-3p alleviated DSS-induced oxidative injury via promoting BRG1-mediated activation Nrf2/HO-1 signaling in NCM460 cells. The in vivo results demonstrated that inhibiting miR-222-3p in IECs significantly relieved oxidative stress and inflammation in the damaged colons of UC and CAC mice, as evidenced by decreases in ROS, MDA, IL-1β and TNF-α levels and increases in GSH-Px levels. Our study further demonstrated that inhibiting miR-222-3p in IECs attenuated oxidative damage by targeting BRG1 to activate the Nrf2/HO-1 signaling. In summary, inhibiting miR-222-3p in IECs attenuates oxidative stress by targeting BRG1 to activate the Nrf2/HO-1 signaling, thereby reducing colonic inflammation and tumorigenesis

Mapping Dirac quasiparticles near a single Coulomb impurity on graphene

The response of Dirac fermions to a Coulomb potential is predicted to differ significantly from how non-relativistic electrons behave in traditional atomic and impurity systems. Surprisingly, many key theoretical predictions for this ultra-relativistic regime have not been tested. Graphene, a two-dimensional material in which electrons behave like massless Dirac fermions, provides a unique opportunity to test such predictions. Graphene’s response to a Coulomb potential also offers insight into important material characteristics, including graphene’s intrinsic dielectric constant, which is the primary factor determining the strength of electron–electron interactions in graphene. Here we present a direct measurement of the nanoscale response of Dirac fermions to a single Coulomb potential placed on a gated graphene device. Scanning tunnelling microscopy was used to fabricate tunable charge impurities on graphene, and to image electronic screening around them for a Q = +1|e| charge state. Electron-like and hole-like Dirac fermions were observed to respond differently to a Coulomb potential. Comparing the observed electron–hole asymmetry to theoretical simulations has allowed us to test predictions for how Dirac fermions behave near a Coulomb potential, as well as extract graphene’s intrinsic dielectric constant: ε[subscript g] = 3.0±1.0. This small value of ε[subscript g] indicates that electron–electron interactions can contribute significantly to graphene properties.United States. Office of Naval Research. Multidisciplinary University Research Initiative (Award N00014-09-1-1066)United States. Dept. of Energy. Office of Science (Contract DE-AC02-05CH11231)National Science Foundation (U.S.) (Award DMR-0906539