Leptin, the product of ob gene, is an endocrine hormone that regulates adipose tissue mass. Recently, leptin has been found to generate a growth signal involving a tyrosine kinase-dependent intracellular pathway and promote angiogenic processes via activation of leptin receptor (Ob-R) in endothelial cells. However, it is not clear how leptin functions to promote multi-step processes involved in the neovascularization at the atherosclerotic plaque. We have examined the expression of matrix metalloproteinases (

Electrochromism, photothermal effect, and thermoelectric properties of hexyl-derivatized poly(3,4-ethylenedioxyselenophene) are investigated by precisely controlling the morphology. These properties are clearly demonstrated by controlling the applied electrical potential of the polymer films. Especially, the doped polymer film at -0.1 V reveals the highest photothermal conversion efficiency and a power factor of 42.5% and 354.7 μW m(-1) K(-2) , respectively. Efficient visible to near-infrared absorption, photon to heat, and heat to electric conversion has been realized in one film that could benefit in exploiting multifunctional film displays, invisible NIR sensors, photodynamic theragnosis, and thermoelectric devices.

Robust thermoelectric harvesting is explored from a proton-doped mixed ionic conductive (PMIC) film under water-harvesting metal organic framework (MOF) film coupled with hydrogel layer (MOF/HG). As a PMIC, highly doped poly(3,4-ethylenedioxythiophene)s with poly(styrene sulfonate) (PEDOT:PSS) is prepared by precisely controlling the proton doping to afford a stable and high thermoelectric PMIC. Among the PMICs, the PEDOT:PSS film doped with 30 wt% of poly(styrene sulfonic acid) (PSSH) recorded a Seebeck coefficient of over 16.2 mV K −1 and a thermal voltage of 81 mV for a temperature gradient (ΔT) of 5 K. The thermal charging on PMICs afforded high thermal voltage and current output, reproducibly, to show cumulative thermoelectric nature. Environmentally sustainable thermoelectric harvesting is achieved from a PMIC under a MOF/HG, prepared by water-harvesting MOF-801 coupled with a HG layer, to provide constant relative humidity of 90% and V oc over 72 h at ambient condition.

Objective To investigate the effect of high glucose and spent peritoneal dialysate on the transforming growth factor-β1 (TGFβ1) synthesis of cultured human peritoneal mesothelial cells (HPMCs) and to examine the effect of costimulation with high glucose or spent dialysate, and cytokines, interleukin-1β (IL-1β), and tumor necrosis factor-α (TNFα) on TGFβ1 synthesis of HPMCs. Design HPMCs were exposed to different concentrations of glucose (30, 60, and 90 mmol/L) or spent peritoneal dialysate for 48 hours in the absence or presence of IL-1β (1 ng/mL) and TNFα (1 ng/mL). TGFβ1 mRNA expression was assessed by Northern blot analysis and TGFβ1 protein release by Western blot analysis and enzymelinked immunosorbent assay (ELISA). Results Exposure of HPMCs to high glucose conditions (30, 60, and 90 mmol/L of D-glucose) induced 2.3-, 3.6-, and 4.0-fold increases in TGFβ1 mRNA expression of HPMC with enhanced TGFβ1 protein synthesis and secretion into the media, whereas there were no significant changes in TGFβ1 synthesis with equimolar concentrations of D-mannitol. Incubation with spent dialysate also significantly increased TGFβ1 mRNA expression and protein secretion compared to control media ( p < 0.05). Stimulation with IL-1β (1 ng/mL) or TNFα (1 ng/mL) resulted in a significant increase in TGFβ1 mRNA expression after 48 hours: 2.7 and 2.1 times the control level, respectively. However, TNFα-induced increase in TGFβ1 mRNA expression was not translated into TGFβ1 protein secretion, while IL-1β stimulation induced a significant increase in TGFβ1 protein secretion as well as TGFβ1 mRNA expression. Combined stimulation by high glucose or spent dialysate, together with IL-1β or TNFα, showed a greater increase in TGFβ1 mRNA expression and protein secretion compared to stimulation by high glucose or spent dialysate alone. Conclusion Our results clearly show that high glucose solution and spent dialysate themselves might be sufficient to stimulate the production of TGFβ1 by peritoneal mesothelial cells. In peritoneal dialysis patients, this state of chronic induction of TGFβ1 is further exacerbated in the presence of peritonitis because of the stimulatory effect of proinflammatory cytokines, resulting in augmented TGFβ1 synthesis, thus promoting peritoneal fibrosis.

A photothermally foldable soft bimorph was prepared via the dry transfer of poly(3,4-ethylenedioxythiophene) (PEDOT) doped with tosylate onto a poly(dimethylsiloxane) film. The photothermal folding was optimized via reversible actuation by controlling the thickness of each layer and the temperature increase to afford large deflection and displacement up to 150°and 420 mm, respectively, upon exposure to near-infrared (NIR) light (808 nm). A two-dimensional array of the bimorph converted into complex three-dimensional architectures, such as a Venus flytrap, under light and reversibly unfolded in the dark. Taking advantage of the photothermal nature of PEDOT, a localized heat pocket was generated inside the folding structure. Thus, a Venus flytrap with a hot pocket reaching 100°C was realized for the first time. The Venus flytrap could trap and move an object within a few seconds of NIR exposure.

Rationale-Recent studies have highlighted important roles of CaMKII in regulating Ca 2+ handling and excitation-contraction coupling. However, the cardiac effect of chronic CaMKII inhibition has not been well understood.Objective-We have tested the alterations of L-type calcium current (I Ca ) and cardiac function in CaMKIIδ knockout (KO) mouse left ventricle (LV).Methods and Results-We used patch clamp method to record I Ca in ventricular myocytes and found that in KO LV, basal I Ca was significantly increased without changing the transmural gradient of I Ca distribution. Substitution of Ba 2+ for Ca 2+ showed similar increase in I Ba . There was no change in the voltage dependence of I Ca activation and inactivation. I Ca recovery from inactivation, however, was significantly slowed. In KO LV, the Ca 2+ -dependent I Ca facilitation (CDF) and I Ca response to isoproterenol (ISO) were significantly reduced. However, ISO response was reversed by β2-adrenergic receptor (AR) inhibition. Western blots showed a decrease in β1-AR and an increase in Ca v 1.2, β2-AR and Gαi3 protein levels. Ca 2+ transient and sarcomere shortening in KO myocytes were unchanged at 1Hz but reduced at 3Hz stimulation. Echocardiography in conscious mice revealed an increased basal contractility in KO mice. However, cardiac reserve to workload and β-adrenergic stimulation was reduced. Surprisingly, KO mice showed a reduced heart rate in response to workload or β-adrenergic stimulation.Conclusions-Our results implicate physiologic CaMKII activity in maintaining normal I Ca , Ca 2+ handling, excitation-contraction coupling and the in vivo heart function in response to cardiac stress.

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