Rapid Dye Regeneration Mechanism of Dye-Sensitized Solar Cells

During the light-harvesting process of dye-sensitized solar cells (DSSCs), the hole localized on the dye after the charge separation yields an oxidized dye, D^+. The fast regeneration of D^+ using the redox pair (typically the I^–/I_(3)^– couple) is critical for the efficient DSSCs. However, the kinetic processes of dye regeneration remain uncertain, still promoting vigorous debates. Here, we use molecular dynamics simulations to determine that the inner-sphere electron-transfer pathway provides a rapid dye regeneration route of ∼4 ps, where penetration of I^− next to D^+ enables an immediate electron transfer, forming a kinetic barrier. This explains the recently reported ultrafast dye regeneration rate of a few picoseconds determined experimentally. We expect that our MD based comprehensive understanding of the dye regeneration mechanism will provide a helpful guideline in designing TiO_2−dye−electrolyte interfacial systems for better performing DSSCs

Electrical Characterization of Proposed Transpositional Acupoints on the Urinary Bladder Meridian in a Rat Model

Specific electrical characteristicsof acupointswere investigated on the urinary bladder (BL) meridian in 14 rats. BL acupointsand non-acupoints on the back were selected and their electrical voltages were measured by using aSPACsystem.The mean voltages of each point or each line were statistically analyzed by using the ANOVA test.The BL meridian showed voltages higher than those of the reference line (P < .05). Bilateral 1st BL lines presented higher voltages than bilateral 2nd BL lines (P < .05). Most BL acupoints had voltageshigher than those for the corresponding reference points (P < .05). In particular, theright BL16 exhibited the biggest difference from the reference point, followed by the left extra BL point-2, the right BL27, the left BL17, and theleft BL45. Additionally, the distributions of neurofilamentsfor several points were investigated by using immunohistochemistry. There was a trend for the BL acupoints to have larger numbers of neurofilaments than the reference points, and that trend seemed to be directly proportional to the difference in voltage between the points.In conclusion, BL acupoints on the back in ratsexhibited specific electric and histologic characteristics. Therefore, those acupointsmay be utilized to investigate the efficacy of acupuncturewith laboratory animals

Suppressive Effect on Lipopolysaccharide-Induced Proinflammatory Mediators by Citrus aurantium L. in Macrophage RAW 264.7 Cells via NF-κB Signal Pathway

Citrus fruits have been used as an edible fruit and a traditional medicine since ancient times. In particular, the peels of immature citrus fruits are used widely in traditional herbal medicine in Korea, as they are believed to contain bioactive components exerting anti-inflammatory activity. This study examined whether the crude methanol extract of Citrus aurantium L. (CME) has a suppressive effect on inducible enzymes and proinflammatory cytokines by inhibiting the NF-κB pathway in LPS-stimulated macrophage RAW 264.7 cells. The cells were pretreated with the indicated concentrations of CME (5, 10, 20, and 50 μg/mL) and then treated with LPS (1 μg/mL). The results showed that CME (10, 20, and 50 μg/mL) inhibited the LPS- (1 μg/mL) induced mRNA and protein expression of iNOS in macrophage Raw 264.7 cells. In addition, the expression of COX-2 was inhibited at the mRNA and protein levels by CME in a dose-dependent manner. The mRNA expression of proinflammatory cytokines, such as TNF-α and IL-6, were markedly reduced by CME (10, 20, and 50 μg/mL). Moreover, CME clearly suppressed the nuclear translocation of the NF-κB p65 subunits, which was correlated with its inhibitory effect on I-κB phosphorylation. These results suggest that CME has anti-inflammatory properties by modulating the expression of COX-2, iNOS, and proinflammatory cytokines, such as TNF-α and IL-6, in macrophage RAW 264.7 cells via the NF-κB pathway

Enhanced cardiac expression of two isoforms of matrix metalloproteinase-2 in experimental diabetes mellitus.

BackgroundDiabetic cardiomyopathy (DM CMP) is defined as cardiomyocyte damage and ventricular dysfunction directly associated with diabetes independent of concomitant coronary artery disease or hypertension. Matrix metalloproteinases (MMPs), especially MMP-2, have been reported to underlie the pathogenesis of DM CMP by increasing extracellular collagen content.PurposeWe hypothesized that two discrete MMP-2 isoforms (full length MMP-2, FL-MMP-2; N-terminal truncated MMP-2, NTT-MMP-2) are induced by high glucose stimulation in vitro and in an experimental diabetic heart model.MethodsRat cardiomyoblasts (H9C2 cells) were examined to determine whether high glucose can induce the expression of the two isoforms of MMP-2. For the in vivo study, we used the streptozotocin-induced DM mouse heart model and age-matched controls. The changes of each MMP-2 isoform expression in the diabetic mice hearts were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Immunohistochemical stains were conducted to identify the location and patterns of MMP-2 isoform expression. Echocardiography was performed to compare and analyze the changes in cardiac function induced by diabetes.ResultsQuantitative RT-PCR and immunofluorescence staining showed that the two MMP-2 isoforms were strongly induced by high glucose stimulation in H9C2 cells. Although no definite histologic features of diabetic cardiomyopathy were observed in diabetic mice hearts, left ventricular systolic dysfunction was determined by echocardiography. Quantitative RT-PCR and IHC staining showed this abnormal cardiac function was accompanied with the increases in the mRNA levels of the two isoforms of MMP-2 and related to intracellular localization.ConclusionTwo isoforms of MMP-2 were induced by high glucose stimulation in vitro and in a Type 1 DM mouse heart model. Further study is required to examine the role of these isoforms in DM CMP

FLT4 as a marker for predicting prognostic risk of refractory acute myeloid leukemia

Treating patients with refractory acute myeloid leukemia (AML) remains challenging. Currently there is no effective treatment for refractory AML. Increasing evidence has demonstrated that refractory/relapsed AML is associated with leukemic blasts which can confer resistance to anticancer drugs. We have previously reported that high expression of Fms-related tyrosine kinase 4 (FLT4) is associated with increased cancer activity in AML. However, the functional role of FLT4 in leukemic blasts remains unknown. Here, we explored the significance of FLT4 expression in leukemic blasts of refractory patients and mechanisms involved in the survival of AML blasts. Inhibition or absence of FLT4 in AML blasts suppressed homing to bone marrow of immunocompromised mice and blocked engraftment of AML blasts. Moreover, FLT4 inhibition by MAZ51, an antagonist, effectively reduced the number of leukemic cell-derived colony-forming units and increased apoptosis of blasts derived from refractory patients when it was co-treated with cytosine arabinoside under vascular endothelial growth factor C, its ligand. AML patients who expressed high cytosolic FLT4 were linked to an AML-refractory status by internalization mechanism. In conclusion, FLT4 has a biological function in leukemogenesis and refractoriness. This novel insight will be useful for targeted therapy and prognostic stratification of AML

Irreversible extinction of ferroelectric polarization in P(VDF-TrFE) thin films upon melting and recrystallization

We observed the irreversible extinction of ferroelectric polarization in spun coated poly(vinylidene fluoride-co-trifluoroethylene) thin films upon melting and recrystallization. We investigate the alteration of the ferroelectric properties correlated with the preferred polymer crystal orientation with respect to the electrodes using grazing incident scattering, spectroscopy, and electron microscopes. Heat treatment above melting point gave rise to the significant reduction of the ferroelectric performance mainly caused by the modification of molecular orientation of polymer crystals whose c and b axes are perpendicular and parallel to the electrode surface, respectively, leading to almost zero effective electric field. (c) 2006 American Institute of Physicsopen464

Chylothorax in Gorham's disease.

A 25-yr-old woman presented with a right pleural effusion. Destruction of 9th through 12th ribs, adjacent vertebral bodies, and transverse processes was noted on plain radiograph and a large low-attenuated, irregular shaped mass lesion with peripheral rim enhancement, destroying vertebral body and transverse process, was revealed on the computed tomographic scan. Magnetic resonance imaging showed high signal on T1- weighted image and iso- and low signal on T2-weighted image for the mass lesion replacing the vertebral bony cortex and marrow space. An open rib biopsy revealed the histopathological changes of Gorham's disease (essential osteolysis), even though only bloody fluid filling the empty space and rib and vertebral transverse process destruction were grossly observed on operation. Even though there was no definite response to radiotherapy and pleurodesis, the patient showed stable condition up to 20 months after diagnosis

Effect of intracoronary adenosine on ergonovine-induced vasoconstricted coronary arteries

Background: This study aimed to evaluate the effect of adenosine on epicardial coronary artery diameterduring ergonovine provocation testing.Methods: A total of 158 patients who underwent an ergonovine provocation test with intracoronaryadenosine injection between 2011 and 2014 were selected. Patients were divided into four groups basedon the severity of percent diameter stenosis following intracoronary ergonovine administration: Group 1,induced spasm &lt; 50%; Group 2, 50–89%; Group 3, 90–99%; and Group 4, total occlusion.Results: Spasm positivity was observed in 44 (27.8%) cases in the study population (mean age, 57.4 ±± 10.7 years). Intracoronary adenosine increased the diameter of the ergonovine-induced epicardialartery by 0.51 ± 0.31 mm, 0.73 ± 0.39 mm, 0.44 ± 0.59 mm, and 0.01 ± 0.04 mm in Groups 1, 2, 3,and 4, respectively. Subsequent administration of nitroglycerin further increased vessel diameter by0.49 ± 0.28 mm, 0.93 ± 0.68 mm, 2.11 ± 1.25 mm, and 2.23 ± 0.69 mm in Groups 1, 2, 3, and 4,respectively. The ratios of adenosine-induced diameter to reference diameter were significantly lowerin patients with spasm positive results (0.68 [0.59–0.76] vs. 0.18 [0.00–0.41], p &lt; 0.001 in the studypopulation; 0.60 [0.54–0.67] vs. 0.40 [0.27–0.44], p &lt; 0.001 in Group 2) with the best cut-off value of0.505 (sensitivity 0.955, specificity 0.921).Conclusions: Intracoronary administration of adenosine dilated the ergonovine-induced vasoconstrictedepicardial coronary artery. The ratio of adenosine-induced diameter to reference diameter wassignificantly lower in patients with spasm positive results