NF-kappaB is a key transcription factor that regulates inflammatory processes. In the present study, we tested the hypothesis that blockade of NF-kappaB ameliorates cardiac remodeling and failure after myocardial infarction (MI). Knockout mice with targeted disruption of the p50 subunit of NF-kappaB (KO) were used to block the activation of NF-kappaB. MI was induced by ligation of the left coronary artery in male KO and age-matched wild-type (WT) mice. NF-kappaB was activated in noninfarct as well as infarct myocardium in WT+MI mice, while the activity was completely abolished in KO mice. Blockade of NF-kappaB significantly reduced early ventricular rupture after MI and improved survival by ameliorating congestive heart failure. Echocardiographic and pressure measurements revealed that left ventricular fractional shortening and maximum rate of rise of left ventricular pressure were significantly increased and end-diastolic pressure was significantly decreased in KO+MI mice compared with WT+MI mice. Histological analysis demonstrated significant suppression of myocyte hypertrophy as well as interstitial fibrosis in the noninfarct myocardium of KO+MI mice. Blockade of NF-kappaB did not ameliorate expression of proinflammatory cytokines in infarct or noninfarct myocardium. In contrast, phosphorylation of c-Jun NH2-terminal kinase was almost completely abolished in KO+MI mice. The present study demonstrates that targeted disruption of the p50 subunit of NF-kappaB reduces ventricular rupture as well as improves cardiac function and survival after MI. Blockade of NF-kappaB might be a new therapeutic strategy to attenuate cardiac remodeling and failure after MI.

The present study suggests that VNS modulates the cardiac redox status and adrenergic drive, and thereby suppresses free radical generation in the failing heart.

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Local hyperthyroidism via transcriptional up-regulation of the Dio2 gene may be an important underlying mechanism for the hypertrophic cardiac remodelling in DCM.

Tumor necrosis factor (TNF)-α induced in damaged myocardium has been considered to be cardiotoxic. TNF-α initiates its biological effects by binding two distinct receptors: R1 (p55) and R2 (p75). Although TNF-α has been shown to be cardiotoxic via R1-mediated pathways, little is known about the roles of R2-mediated pathways in myocardial infarction (MI). We created MI in R1 knockout (R1KO), R2KO, and wild-type (WT) mice by ligating the left coronary artery. Functional, histological, and biochemical analyses were performed 4 wk after ligation. Although infarct size was not different among WT, R1KO, and R2KO mice, post-MI survival was significantly improved in R1KO but not R2KO mice. R1KO significantly ameliorated contractile dysfunction after MI, whereas R2KO significantly exaggerated ventricular dilatation and dysfunction. Myocyte hypertrophy and interstitial fibrosis in noninfarct myocardium was exacerbated in R2KO but not in R1KO mice. Expression of R1, which was not affected by MI and was nullified in R1KO mice, was significantly upregulated in R2KO mice. In contrast, expression of R2, which was significantly upregulated by MI and was nullified in R2KO mice, was unaffected in R1KO mice. Meanwhile, TNF-α expression, which was significantly upregulated in noninfarct myocardium after MI, was not affected by R1KO or R2KO. However, transcript levels of IL-6, IL-1β, transforming growth factor-β, and monocyte chemotactic protein-1, which were significantly upregulated after MI, were significantly downregulated in R1KO mice. In contrast, transcript levels of IL-6 and IL-1β were significantly further upregulated in R2KO mice. TNF-α is toxic via R1 and protective via R2 in a murine model of MI. Selective blockade of R1 may be a candidate therapeutic intervention for MI.

Graphenes of nanometer-scale grain size (nanographenes) were synthesized using in-liquid plasmas with alcohols or hydrocarbons. This method of nanographene synthesis showed a trade-off relationship between crystallinity and synthesis rate. The high crystallinity of nanographenes synthesized with alcohols was evaluated from the small full width at half maxima (FWHM) of the G band in Raman scattering spectra. On the other hand, in the case of using hydrocarbons such as n-hexane and benzene, a significantly high synthesis rate was obtained but the crystallinity of nanographenes was low. It was found that hydroxyl groups and oxygen atoms of liquid sources play important roles in determining the crystallinity of synthesized nanographenes.

The atomic layer etching (ALE) of silicon nitride (SiN) via a hydrogen plasma followed by exposure to fluorine radicals was investigated by using in situ spectroscopic ellipsometry and attenuated total reflectance Fourier transform infrared (FTIR) spectroscopy to examine the surface reactions and etching mechanism. FTIR spectra of the surface following exposure to the hydrogen plasma showed an increase in the concentration of Si−H and N−H bonds, although the N−H bond concentration plateaued more quickly. In contrast, during fluorine radical exposure, the Si−H bond concentration decreased more rapidly. Secondary ion mass spectrometry demonstrated that the nitrogen atom concentration was decreased to a depth of 4 nm from the surface after the hydrogen plasma treatment and indicated a structure consisting of N−H rich, Si−H rich, and mixed layers. This indicated that Si−H bonds were primarily present near the surface, while N−H bonds were mainly located deeper into the film. The formations of the N−H and Si−H rich layers are important phenomena associated with modification by hydrogen plasma and fluorine radical etching, respectively.

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