Nanograting formation on metals in air with interfering femtosecond laser pulses

It is demonstrated that a homogeneous nanograting having the groove period much smaller than the laser wavelength (∼800 nm) can be fabricated on metals in air through ablation induced by interfering femtosecond laser pulses (100 fs at a repetition rate of 10 Hz). Morphological changes on stainless steel and Ti surfaces, observed with an increase in superimposed shots of the laser pulses at a low fluence, have shown that the nanograting is developed through bonding structure change at the interference fringes, plasmonic near-field ablation to create parallel grooves on the fringe, and subsequent excitation of surface plasmon polaritons to regulate the groove intervals at 1/3 or 1/4 of the fringe period over the whole irradiated area. Calculation for a model target having a thin oxide layer on the metal substrate reproduces well the observed groove periods and explains the mechanism for the nanograting formation

Aerosol Characteristics of Admixture of Budesonide Inhalation Suspension with a Beta2-Agonist, Procaterol

Background: Nebulized drugs for asthma treatment are often mixed together in order to simplify inhalation regimens, although not recommended. We therefore evaluated aerosol characteristics and physicochemical stability of the admixture of an inhaled corticosteroid suspension with a beta2-agonist solution. Methods: An 8-stage cascade impactor was used to measure the particle size distribution of admixture of Pulmicort® Respules® (budesonide, 0.5 mg/2 mL) with Meptin® Inhalation Solution Unit (procaterol hydrochloride, 30 Mg/0.3 mL) from a jet nebulizer, PARI LC Plus®. Concentration of each drug was assayed with high- pressure liquid chromatography. Physicochemical compatibility was also assessed up to 24 hours after mixing. Results: With regard to budesonide, impactor parameters such as mass median aerodynamic diameter (MMAD) and respirable mass (RM) were comparable between admixtures and single-drug preparations (2.92 ± 0.03 vs 2.99 ± 0.14 µm, 146.8 ± 2.9 vs 147.6 ± 8.2 µg, respectively). On the other hand, delivery rates of procaterol increased when admixed with budesonide suspension, resulting in significantly higher RM (15.1 ± 0.8 vs 10.2 ± 0.5 µg, p < 0.01). Variations from initial concentration in the percentages of drug remaining at any time point were less than 10%, and there were no appreciable changes in pH of the admixtures for up to 24 hours. Conclusions: There is a possibility that admixture might influence of aerodynamic characteristics of procaterol, but not budesonide. In vivo data will be needed for the clinical implications of our findings

Plasma diamine oxidase activity in asthmatic children

Histamine plays an important role in the development of asthmatic symptoms. Diamine oxidase (DAO histaminase), which inactivates histamine, is located in the intestine and kidney and is released into plasma. Plasma DAO activity in asthmatic children was measured by a recently developed high performance liquid chromatographic method using histamine as the DAO substrate. Diamine oxidase activity was higher in severely asthmatic children than in those with mild asthma. A time course study during the acute exacerbation phase revealed that DAO activity rose during acute asthmatic attacks and then decreased gradually over several days. Although the mechanisms of plasma DAO activity increase during acute asthmatic attacks could not be explained, data showed that plasma DAO activity is an important index of histamine metabolism in asthmatics and may relate to some mechanisms of acute exacerbation of airway inflammation. Consequently, fluctuations in plasma DAO can be used as one of various indices of instability in management of asthma

Central Insulin Action Activates Kupffer Cells by Suppressing Hepatic Vagal Activation via the Nicotinic Alpha 7 Acetylcholine Receptor

Central insulin action activates hepatic IL-6/STAT3 signaling, which suppresses the gene expression of hepatic gluconeogenic enzymes. The vagus nerve plays an important role in this centrally mediated hepatic response; however, the precise mechanism underlying this brain-liver interaction is unclear. Here, we present our findings that the vagus nerve suppresses hepatic IL-6/STAT3 signaling via α7-nicotinic acetylcholine receptors (α7-nAchR) on Kupffer cells, and that central insulin action activates hepatic IL-6/STAT3 signaling by suppressing vagal activity. Indeed, central insulin-mediated hepatic IL-6/STAT3 activation and gluconeogenic gene suppression were impeded in mice with hepatic vagotomy, pharmacological cholinergic blockade, or α7-nAchR deficiency. In high-fat diet-induced obese and insulin-resistant mice, control of the vagus nerve by central insulin action was disturbed, inducing a persistent increase of inflammatory cytokines. These findings suggest that dysregulation of the α7-nAchR-mediated control of Kupffer cells by central insulin action may affect the pathogenesis of chronic hepatic inflammation in obesity